Environmental Microbial Exposure Research Articles

Early-life nasal microbiota dynamics relate to longitudinal respiratory phenotypes in urban children

Five distinct respiratory phenotypes based on latent classes of longitudinal patterns of wheezing, allergic sensitization. and pulmonary function measured in urban children from ages from 0 to 7 years have previously been described. Our aim was to determine whether distinct respiratory phenotypes are associated with early-life upper respiratory microbiota development and environmental microbial exposures. Microbiota profiling was performed using 16S ribosomal RNA-based sequencing of nasal samples collected at age 12 months (n= 120) or age 36 months (n= 142) and paired house dust samples collected at 3 months (12-month, n= 73; 36-month, n= 90) from all 4 centers in the Urban Environment and Childhood Asthma (URECA) cohort. In these high-risk urban children, nasal microbiota increased in diversity between ages 12 and 36 months (ß= 2.04; P= .006). Age-related changes in microbiota evenness differed significantly by respiratory phenotypes (interaction P= .0007), increasing most in the transient wheeze group. At age 12 months, respiratory illness (R2= 0.055; P= .0001) and dominant bacterial genus (R2= 0.59; P= .0001) explained variance in nasal microbiota composition, and enrichment of Moraxella and Haemophilus members was associated with both transient and high-wheeze respiratory phenotypes. By age 36months, nasal microbiota was significantly associated with respiratory phenotypes (R2= 0.019; P= .0376), and Moraxella-dominated microbiota was associated specifically with atopy-associated phenotypes. Analysis of paired house dust and nasal samples indicated that 12 month olds with low wheeze and atopy incidence exhibited the largest number of shared bacterial taxa with their environment. Nasal microbiota development over the course of early childhood and composition at age 3 years are associated with longitudinal respiratory phenotypes. These data provide evidence supporting an early-life window of airway microbiota development that is influenced by environmental microbial exposures in infancy and associates with wheeze- and atopy-associated respiratory phenotypes through age 7 years.

Spraying compound probiotics improves growth performance and immunity and modulates gut microbiota and blood metabolites of suckling piglets.

One factor that shapes the establishment of early neonatal intestinal microbiota is environmental microbial exposure, and probiotic application has been shown to promote health and growth of piglets. Thus, this study hypothesized that environmental probiotic application in early days of life would be beneficial to newborn piglets. This study aimed to investigate the effect of spraying a compound probiotic fermented liquid (CPFL) into the living environment of piglets on their early growth performance and immunity. This work included 68 piglets, which were randomized into probiotic and control groups. Blood and fecal samples were collected at 0, 3, 7, 14, and 21 days of age. Spraying CPFL significantly reshaped the microbiota composition of the delivery room environment, increased piglets' daily weight gain and weaning weight (P<0.001), and modulated piglets' serum cytokine levels (increases in IgA, IgG, and IL-10; decrease in IFN-γ; P<0.05 in each case) in piglets. Additionally, spraying CPFL during early days of life modified piglets' gut microbiota structure and diversity, increased the abundance of some potentially beneficial bacteria (such as Bacteroides uniformis, Butyricimonas virosa, Parabacteroides distasonis, and Phascolarctobacterium succinatutens) and decreased the abundance of Escherichia coli (P<0.05). Interestingly, CPFL application also significantly enhanced the gut microbial bioactive potential and levels of several serum metabolites involved in the metabolism of vitamins (B2, B3, B6, and E), medium/long-chain fatty acids (caproic, tetradecanoic, and peptadecanoic acids), and dicarboxylic acids (azelaic and sebacic acids). Our study demonstrated that spraying CPFL significantly could improve piglets' growth performance and immunity, and the beneficial effects are associated with changes in the gut microbiota and host metabolism. Our study has provided novel data for future development of probiotic-based health-promoting strategies and expanded our knowledge of probiotic application in animal husbandry.

Limited microbiome differences in captive and semi-wild primate populations consuming similar diets.

Gut microbial communities are shaped by a myriad of extrinsic factors, including diet and the environment. Although distinct human populations consistently exhibit different gut microbiome compositions, variation in diet and environmental factors are almost always coupled, making it difficult to disentangle their relative contributions to shaping the gut microbiota. Data from discrete animal populations with similar diets can help reduce confounds. Here, we assessed the gut microbiota of free-ranging and captive rhesus macaques with at least 80% diet similarity to test the hypothesis that hosts in difference environments will have different gut microbiomes despite a shared diet. Although we found that location was a significant predictor of gut microbial composition, the magnitude of observed differences was relatively small. These patterns suggest that a shared diet may limit the typical influence of environmental microbial exposure on the gut microbiota.

The role of LPS and CpG in the farm effect against allergies, and beyond.

The prevalence of allergic disease has increased significantly over the past decades. Although allergies are inherently multifactorial and heterogenous; environmental, maternal, and early-life microbial exposures could strongly modify disease risk. The effects of environmental microbiota are illustrated by the “farm effect”, showing protection against asthma when children grow up on traditional farms. Recent studies have further revealed an important role for early-life exposure to a microbe-rich environment imposing lung and gut microbiome maturation and immune education, preventing allergic disease in childhood. Advances are made in the field of immunology and microbiome research, which identified entire microbial taxa, as well as specific microbial metabolites and bacterial products associated with reducing disease risk. Here we discuss the cross-talk between the microbiota and the pathogenesis of allergic disease, including bacterial products as lipopolysaccharide and CpG, in the farm effect.

Infant pacifier sanitization and risk of challenge-proven food allergy: A cohort study

Environmental microbial exposure plays a role in immune system development and susceptibility to food allergy. We sought to investigate whether infant pacifier use during the first postnatal year, with further consideration of sanitization, alters the risk of food allergy by age 1 year. The birth cohort recruited pregnant mothers at under 28 weeks' gestation in southeast Australia, with 894 families followed up when infants turned 1 year. Infants were excluded if born under 32 weeks, with a serious illness, major congenital malformation, or genetic disease. Questionnaire data, collected at recruitment and infant ages 1, 6, and 12 months, included pacifier use and pacifier sanitization (defined as the joint exposure of a pacifier and cleaning methods). Challenge-proven food allergy was assessed at 12 months. Any pacifier use at 6 months was associated with food allergy (adjusted odds ratio, 1.94; 95% CI, 1.04-3.61), but not pacifier use at other ages. This overall association was driven by the joint exposure of pacifier-antiseptic use (adjusted odds ratio, 4.83; 95% CI, 1.10-21.18) compared with no pacifier use. Using pacifiers without antiseptic at 6 months was not associated with food allergy. Among pacifier users, antiseptic cleaning was still associated with food allergy (adjusted odds ratio, 3.56; 95% CI, 1.18-10.77) compared with no antiseptic use. Furthermore, persistent and repeated antiseptic use over the first 6 months was associated with higher food allergy risk (P= .029). This is the first report of a pacifier-antiseptic combination being associated with a higher risk of subsequent food allergy. Future work should investigate underlying biological pathways.

Simultaneous allergic traits in dogs and their owners are associated with living environment, lifestyle and microbial exposures

Both humans and pet dogs are more prone to develop allergies in urban than in rural environments, which has been associated with the differing microbial exposures between areas. However, potential similarities in the microbiota, that associate with environmental exposures, in allergic dogs and owners has not been investigated. We evaluated skin and gut microbiota, living environment, and lifestyle in 168 dog-owner pairs. Due to partly different manifestations of allergies between species, we focused on aeroallergen sensitized humans and dogs with owner-reported allergic symptoms. Our results agree with previous studies: dog-owner pairs suffered simultaneously from these allergic traits, higher risk associated with an urban environment, and the skin, but not gut, microbiota was partly shared by dog-owner pairs. We further discovered that urban environment homogenized both dog and human skin microbiota. Notably, certain bacterial taxa, which were associated with living environment and lifestyle, were also related with allergic traits, but these taxa differed between dogs and humans. Thus, we conclude that dogs and humans can be predisposed to allergy in response to same risk factors. However, as shared predisposing or protective bacterial taxa were not discovered, other factors than environmental microbial exposures can mediate the effect or furry dog and furless human skin select different taxa.

Natural History and Risk Factors of Infantile Atopic Dermatitis: A Case Report and Literature Review

Atopic dermatitis (AD) or atopic eczema is one of the most common forms of pediatric dermatological skin conditions, primarily beginning in childhood with a variable natural course characterized by intense pruritus and eczematous lesions. This condition requires multifactorial interplay and risk factors to explain the pathogenesis. We hereby report a case of a two-month-old male who presented with widespread erythematous lesions, excoriations, and dry skin since one day before admission. The antenatal history showed use of antibiotics during pregnancy, familial history of atopy, and non-exclusive breastfeeding which are all known risk factors. Dermatological examination revealed skin phototype III with diffuse erythematous patches scattered on the face, trunk, upper and lower limbs, and groin followed with excoriations and palmar hyperlinearity. Further laboratory and histopathological examinations were not conducted. The patient was treated with topical corticosteroid and emollients, resulting in a notable improvement without any further flares. A thorough history taking and physical examination must be conducted to establish the diagnosis based on the Hanifin and Rajka criteria and identify risk factors such as genetic factors, impaired skin barrier, and environmental factors and microbial exposure, which may play a protective or harmful role in AD development. Holistic treatments consist of pharmacological and non-pharmacological treatments, with significant emphasis on education to the patient and caregiver(s) to improve quality of life and prevent exacerbations and infectious complications while minimizing potential medication side effects.

Transfer of environmental microbes to the skin and respiratory tract of humans after urban green space exposure

BackgroundIn industrialized countries, non-communicable diseases have been increasing in prevalence since the middle of the 20th century. While the causal mechanisms remain poorly understood, increased population density, pollution, sedentary behavior, smoking, changes in diet, and limited outdoor exposure have all been proposed as significant contributors. Several hypotheses (e.g. Hygiene, Old Friends, and Biodiversity Hypotheses) also suggest that limited environmental microbial exposures may underpin part of this rise in non-communicable diseases. In response, the Microbiome Rewilding Hypothesis proposes that adequate environmental microbial exposures could be achieved by restoring urban green spaces and could potentially decrease the prevalence of non-communicable diseases. However, the microbial interactions between humans and their surrounding environment and the passaging of microbes between both entities remains poorly understood, especially within an urban context. ResultsHere, we survey human skin (n = 90 swabs) and nasal (n = 90 swabs) microbiota of three subjects that were exposed to air (n = 15), soil (n = 15), and leaves (n = 15) from different urban green space environments in three different cities across different continents (Adelaide, Australia; Bournemouth, United Kingdom; New Delhi, India). Using 16S ribosomal RNA metabarcoding, we examined baseline controls (pre-exposure) of both skin (n = 16) and nasal (n = 16) swabs and tracked microbiota transfer from the environment to the human body after exposure events. Microbial richness and phylogenetic diversity increased after urban green space exposure in skin and nasal samples collected in two of the three locations. The microbial composition of skin samples also became more similar to soil microbiota after exposure, while nasal samples became more similar to air samples. Nasal samples were more variable between sites and individuals than skin samples. ConclusionsWe show that exposure to urban green spaces can increase skin and nasal microbial diversity and alter human microbiota composition. Our study improves our understanding of human-environmental microbial interactions and suggests that increased exposure to diverse outdoor environments may increase the microbial diversity, which could lead to positive health outcomes for non-communicable diseases.

COVID 19 mortality: Probable role of microbiome to explain disparity

There is a significant difference between COVID 19 associated mortality between different countries. Generally the number of deaths per million population are higher in the developed countries despite better health care efficiency, drinking water quality and expected healthy life span (HALE) at the time of birth. Developing and underdeveloped countries on the other hand have lower mortality even with higher rural and slum populations along with incidence of diarrhea because of lack of sanitation. We analyzed data from 122 countries out of which 80 were high or upper middle income and 42 were low or low middle income countries. There was statistically significant positive correlation between COVID 19 deaths /million population and water current score, health efficiency, and HALE. Statistically significant negative correlation was observed with % rural population and fraction of diarrhea because of inadequate sanitation for all ages. Moreover analysis of 51 countries showed that there is significant negative correlation between COVID 19 deaths /million population and proportion of total population living in slums. We propose that high microbial exposure particularly gram negative bacteria can possibly induce interferon type I which might have a protective effect against COVID 19 since the countries with less mortality also tend to have lack of sanitation and high incidence of attendant diseases. So, far none of the predictive models have taken into account immune status of populations engendered by environmental microbial exposure or microbiome. There might be a need to look at dynamics of COVID 19 pandemic using immune perspective. The approach can potentially inform better policies including interventions.

Ecological interactions in asthma: from environment to microbiota and immune responses.

Asthma is a heterogeneous condition shaped not only by genetics but also host conditioning by environmental factors. Recognizing the ecological context of microbe-immune interactions across environments and body sites is a necessary step toward better understanding how human microbiota influence or drive the pathogenesis and pathophysiology of asthma in its various presentations. There is increasing evidence of a critical role for microbiota in asthma pathogenesis and outcomes across various body compartments, including the upper and lower airways, and gut. We discuss recent studies from this area including: development of a method to quantify microbial farm-effect in nonfarm environments, relationships between environmental microbial exposures and asthma prevalence across different geographies, microbiome-mediated responses to ozone, and microbiome-immune interactions within and across body compartments. Beyond bacteria, recent reports of asthma-associated differences in archaea and fungal organisms also are highlighted. Collective evidence warrants application of an ecological framework to advance mechanistic insights into microbiota-immune interactions in asthma. This is necessary to achieve goals of developing successful therapeutic interventions targeting modification of microbiomes.

Household dampness and microbial exposure related to allergy and respiratory health in Danish adults

ABSTRACT Background Indoor dampness has consistently been associated with respiratory symptoms and exacerbations. The causal mechanisms may involve increased microbial exposures. However, the evidence regarding the influence of indoor microbial exposures under damp- and non-damp conditions on the risk of asthma and allergy has been inconclusive. Objective The aim of this study was to investigate the association between dampness and microbial exposure with allergy and respiratory health in Danish adults using a cross-sectional design. Methods From 1,866 participants of the Health2006 cohort, we selected three non-overlapping groups: 196 at random, 107 with confirmed atopy, and 99 without atopy. Bedroom dust was sampled using electrostatic dust fall collectors and analysed for endotoxin, β-(1,3)-D-glucan, 19 microbial species or groups, and total fungal load. Household moisture-related problems and asthma were self-reported by questionnaire. Atopy was determined by skin-prick-testing and lung function was measured by spirometry. Results Household moisture damage was positively associated with asthma outcomes, although this was statistically significant only in atopics for self-reported asthma (odds ratio (OR) 3.52; 95%CI 1.01–12.7). Mould odor was positively associated with wheezing (OR 6.05; 95%CI 1.19–30.7) in atopics. Inconsistent associations were found for individual microbial exposures and health outcomes. Inverse associations were observed between microbial diversity and rhinitis in the random sample and both doctor-diagnosed and self-reported asthma in non-atopics. Conclusions In conclusion, our findings suggest that household moisture damage may increase the risk of asthma and wheeze with mould odor in atopics. In addition, asthma and allergy may be affected by the indoor microbial composition in urban domestic environments. Further studies are needed to identify and understand the causal agents and underlying mechanisms behind the potential effects of environmental microbial exposure on human health.

Naturally-diverse airborne environmental microbial exposures modulate the gut microbiome and may provide anxiolytic benefits in mice

Growing epidemiological evidence links natural green space exposure with a range of health benefits, including for mental health. Conversely, greater urbanisation associates with increased risk of mental health disorders. Microbiomes are proposed as an important but understudied link that may help explain many green space-human health associations. However, there remains a lack of controlled experimental evidence testing possible beneficial effects from passive exposure to natural biodiversity via airborne microbiota. Previous mouse model studies have used unrealistic environmental microbial exposures—including excessive soil and organic matter contact, feed supplements and injections—to demonstrate host microbiota, immune biomarker, and behavioural changes. Here, in a randomised controlled experiment, we demonstrate that realistic exposures to trace-level dust from a high biodiversity soil can change mouse gut microbiota, in comparison to dust from low biodiversity soil or no soil (control) (n = 54 total mice, comprising 3 treatments × 18 mice, with 9 females + 9 males per group). Furthermore, we found a nominal soil-derived anaerobic spore-forming butyrate-producer, Kineothrix alysoides, was supplemented to a greater extent in the gut microbiomes of high biodiversity treatment mice. Also, increasing relative abundance of this rare organism correlated with reduced anxiety-like behaviour in the most anxious mice. Our results point to an intriguing new hypothesis: that biodiverse soils may represent an important supplementary source of butyrate-producing bacteria capable of resupplying the mammalian gut microbiome, with potential for gut health and mental health benefits. Our findings have potential to inform cost-effective population health interventions through microbiome-conscious green space design and, ultimately, the mainstreaming of biodiversity into health care.

Impact of environmental microbiota on human microbiota of workers in academic mouse research facilities: An observational study

ObjectivesTo characterize the microbial environment of workers in academic mouse research facilities using endotoxin, 16S qPCR, and 16S amplicon sequencing. To determine whether the work microbiome contributes to the human microbiome of workers.MethodsWe performed area air sampling from the animal rooms, dirty, middle, and setup cage wash locations in four academic mouse research facilities. 10 workers in the dirty cage wash area underwent personal air sampling as well as repeated collection of nasal, oral, and skin samples before and after the work shift. Environmental samples underwent measurement of endotoxin, mouse allergen, bacteria copy number via 16S qPCR, and microbial identification via 16S rDNA sequencing. 16S rDNA sequencing was also performed on human samples before and after the work shift. SourceTracker was used to identify the contribution of the work microbiome to the human microbiome.ResultsMedian endotoxin levels ranged from undetectable to 1.0 EU/m3. Significant differences in mouse allergen levels, bacterial copy number, microbial richness, and microbial community structure were identified between animal, dirty, middle, and setup cage wash locations. Endotoxin levels had only a moderate correlation with microbial composition. Location within a facility was a stronger predictor of microbial community composition (R2 = 0.41, p = 0.002) than facility. The contribution of the work microbiome to the pre-shift human microbiome of workers was estimated to be 0.1 ± 0.1% for the oral microbiome; 3.1 ± 1.9% for the nasal microbiome; and 3.0 ± 1.5% for the skin microbiome.ConclusionsThe microbial environment of academic animal care facilities varies significantly by location rather than facility. Endotoxin is not a proxy for assessment of environmental microbial exposures using 16S qPCR or 16S rDNA sequencing. The work microbiome contributes to the composition of the nasal and skin microbiome of workers; the clinical implications of this observation should be further studied.

Impact of Rural and Urban Environmental Microbial Exposure on Intestinal Microbiota in Early Infancy

Impact of Rural and Urban Environmental Microbial Exposure on Intestinal Microbiota in Early Infancy

Gut Microbiota and Allergic Disease. New Insights.

The rapid rise in childhood allergies (atopy) in Westernized nations has implicated associated environmental exposures and lifestyles as primary drivers of disease development. Culture-based microbiological studies indicate that atopy has demonstrable ties to altered gut microbial colonization in very early life. Infants who exhibit more severe multisensitization to food- or aero-allergens have a significantly higher risk of subsequently developing asthma in childhood. Hence an emerging hypothesis posits that environment- or lifestyle-driven aberrancies in the early-life gut microbiome composition and by extension, microbial function, represent a key mediator of childhood allergic asthma. Animal studies support this hypothesis. Environmental microbial exposures epidemiologically associated with allergy protection in humans confer protection against airway allergy in mice. In addition, gut microbiome-derived short-chain fatty acids produced from a high-fiber diet have been shown to protect against allergy via modulation of both local and remote mucosal immunity as well as hematopoietic antigen-presenting cell populations. Here we review key data supporting the concept of a gut-airway axis and its critical role in childhood atopy.

Quantity and Diversity of Environmental Microbial Exposure and Development of Asthma: A Birth Cohort Study

AM Karvonen, A Hyvarinen, H Rintala. Allergy. 2014;69(8):1092–1101 The goal of this study was to identify better ways to characterize microbial exposure early in life as a possible predictor of respiratory symptoms and allergies. A birth cohort of 410 children in Finland was recruited over a 3-year period and followed up until 6 years of age. Asthma, wheezing, cough, and atopic dermatitis were assessed by questionnaires administered during the third trimester and in follow-up at ages 2, …

Microbiome in Inner‐City Asthma

Prevalence of childhood asthma has increased dramatically over the past several decades in Western nations, and particularly in inner city populations. Evidence has emerged for both local environmental exposure in infancy and early life gut microbiome disturbances as associated with childhood allergic asthma development. This has led to the hypothesis that the house dust microbial environment of infants may influence their developing gut microbiome in a manner that alters the risk for childhood allergic disease and asthma development. We have recently demonstrated that house dust microbiome composition varies across inner‐city homes and that this variability is significantly related to allergic disease development in children raised in these environments. Children who develop atopy and recurrent wheezing at age three lack environmental microbial exposures in their house dust that are encountered by children who do not develop these disease phenotypes. The majority of these organisms enriched in allergy‐protective households have been previously described in the human gut microbiome. Moreover, murine studies have demonstrated that exposure of mice to dust from allergy protective households, alters the composition of the gut microbiome in a manner that protects against airway allergen challenge. A specific species, Lactobacillus sakei, found to be significantly enriched in the gut microbiome of these protected animals, was capable of conferring airway protection against both allergen and respiratory viral infection in animals supplemented orally with this species. Hence the growing evidence supports a strong role for household microbial exposures as playing a role in shaping gut microbiome composition in early infancy, in a manner that influences mucosal adaptive responses to a variety of airway insults.

Quantity and diversity of environmental microbial exposure and development of asthma: a birth cohort study.

BackgroundEarly-life exposure to environmental microbial agents may be associated with the development of allergies. The aim of the study was to identify better ways to characterize microbial exposure as a predictor of respiratory symptoms and allergies.MethodsA birth cohort of 410 children was followed up until 6 years of age. Bacterial endotoxin, 3-hydroxy fatty acids, N-acetyl-muramic acid, fungal extracellular polysaccharides (EPS) from Penicillium and Aspergillus spp., β-D-glucan, ergosterol, and bacterial or fungal quantitative polymerase chain reactions (qPCRs) were analyzed from dust samples collected at 2 months of age. Asthma, wheezing, cough, and atopic dermatitis were assessed using repeated questionnaires. Specific IgEs were determined at the age of 1 and 6 years.ResultsOnly few associations were found between single microbial markers and the studied outcomes. In contrast, a score for the total quantity of microbial exposure, that is, sum of indicators for fungi (ergosterol), Gram-positive (muramic acid) bacteria, and Gram-negative (endotoxin) bacteria, was significantly (inverted-U shape) associated with asthma incidence (P < 0.001): the highest risk was found at medium levels (adjusted odds ratio (aOR) 2.24, 95% confidence interval (95% CI) 0.87–5.75 for 3rd quintile) and the lowest risk at the highest level (aOR 0.34, 95% CI 0.09–1.36 for 5th quintile). The microbial diversity score, that is, sum of detected qPCRs, was inversely associated with risk of wheezing and was significantly (inverted-U shape) associated with sensitization to inhalant allergens.ConclusionScore for quantity of microbial exposure predicted asthma better than single microbial markers independently of microbial diversity and amount of dust. Better indicators of total quantity and diversity of microbial exposure are needed in studies on the development of asthma.

The Intestinal Metabolome: An Intersection Between Microbiota and Host

Recent advances that allow us to collect more data on DNA sequences and metabolites have increased our understanding of connections between the intestinal microbiota and metabolites at a whole-systems level. We can also now better study the effects of specific microbes on specific metabolites. Here, we review how the microbiota determines levels of specific metabolites, how the metabolite profile develops in infants, and prospects for assessing a person's physiological state based on their microbes and/or metabolites. Although data acquisition technologies have improved, the computational challenges in integrating data from multiple levels remain formidable; developments in this area will significantly improve our ability to interpret current and future data sets.

Passive maternal exposure to environmental microbes selectively modulates the innate defences of chicken egg white by increasing some of its antibacterial activities.

BackgroundEgg defence against bacterial contamination relies on immunoglobulins (IgY) concentrated in the yolk and antimicrobial peptides/proteins predominantly localized in the egg white (EW). Hens contaminated with pathogenic microorganisms export specific IgYs to the egg (adaptative immunity). No evidence of such regulation has been reported for the antimicrobial peptides/proteins (innate immunity) which are preventively secreted by the hen oviduct and are active against a large range of microbes. We investigated whether the egg innate defences can be stimulated by the environmental microbial contamination by comparing the antimicrobial activity of EW of hens raised in three extreme breeding conditions: Germ-free (GF), Specific Pathogen Free (SPF) and Conventional (C) hens.ResultsThe difference in the immunological status of GF, SPF and C hens was confirmed by the high stimulation of IL-1β, IL-8 and TLR4 genes in the intestine of C and SPF groups. EW from C and SPF groups demonstrated higher inhibitory effect against Staphylococcus aureus (13 to 18%) and against Streptococcus uberis (31 to 35%) as compared to GF but showed similar activity against Salmonella Enteritidis, Salmonella Gallinarum, Escherichia coli and Listeria monocytogenes. To further investigate these results, we explored putative changes amongst the three main mechanisms of egg antimicrobial defence: the sequestration of bacterial nutrients, the inactivation of exogenous proteases and the direct lytic action on microorganisms. Lysozyme activity, chymotrypsin-, trypsin- and papain-inhibiting potential of EW and the expression of numerous antimicrobial genes were not stimulated suggesting that these are not responsible for the change in anti-S. aureus and anti-S. uberis activity. Moreover, whereas the expression levels of IL-1β, IL-8 and TLR4 genes were modified by the breeding conditions in the intestine of C and SPF groups they were not modified in the magnum where egg white is formed.ConclusionsAltogether, these data revealed that the degree of environmental microbial exposure of the hen moderately stimulated the egg innate defence, by reinforcing some specific antimicrobial activities to protect the embryo and to insure hygienic quality of table eggs.