Number Of Intestinal Lymphocytes Research Articles

Porcine kobuvirus enhances porcine epidemic diarrhea virus pathogenicity and alters the number of intestinal lymphocytes in piglets

Recent epidemiological studies have discovered that a lot of cases of porcine epidemic diarrhea virus (PEDV) infection are frequently accompanied by porcine kobuvirus (PKV) infection, suggesting a potential relationship between the two viruses in the development of diarrhea. To investigate the impact of PKV on PEDV pathogenicity and the number of intestinal lymphocytes, piglets were infected with PKV or PEDV or co-infected with both viruses. Our findings demonstrate that co-infected piglets exhibit more severe symptoms, acute gastroenteritis, and higher PEDV replication compared to those infected with PEDV alone. Notably, PKV alone does not cause significant intestinal damage but enhances PEDV's pathogenicity and alters the number of intestinal lymphocytes. These results underscore the complexity of viral interactions in swine diseases and highlight the need for comprehensive diagnostic and treatment strategies addressing co-infections.

Interleukin 15 and CD4+ T Cells Cooperate to Promote Small Intestinal Enteropathy in Response to Dietary Antigen

CD4(+) T cells specific for dietary gluten and interleukin 15 (IL15) contribute to the pathogenesis of celiac disease. We investigated whether and how they interact to damage the intestine using mice that overexpress human IL15 in the intestinal epithelium and have CD4(+) T cells specific for ovalbumin, a dietary antigen. We crossed mice with CD4(+) T cells specific for ovalbumin (OTII) with mice that overexpress human IL15 under an intestine-specific promoter (B6× IL15Tge). The offspring (OTII× IL15Tge mice) received control or ovalbumin-containing diets until 3 months of age. Enteropathy was monitored by weight, ratio of villous:crypt length, and the number of intestinal lymphocytes. Phenotype, cytokine production, and degranulation of mucosal and spleen lymphocytes were analyzed by multicolor flow cytometry or enzyme-linked immunosorbent assay. Regulatory T-cell function and CD8(+) T-cell activation were analyzed in co-culture assays. Exposure to ovalbumin reduced growth and led to enteropathy in OTII× IL15Tge mice but not in control OTII× B6 littermates. Enteropathy was associated with expansion of mucosal granzyme B(+) CD8(+) T cells, and developed despite increased frequency of functional ovalbumin-specific regulatory T cells. Ovalbumin-activated CD4(+) T cells secreted IL2, which along with IL15 stimulated expansion of noncognate intestinal cytotoxic CD8(+) T cells, which did not respond to regulatory T cells and induced epithelial damage. We observed that in mice given food antigen, cooperation between IL15 and CD4(+) T cells is necessary and sufficient to activate CD8(+) T cells and damage the small intestine. We propose that this process is involved in the development of celiac disease.

Role of mesenteric lymph pathway in the effects of exogenous somatostatin against early intestinal injury after ischemia–reperfusion in rats

Intestinal ischemia–reperfusion (I/R)-induced gut injury remains a challenge for critically ill patients. This study aims to test whether mesenteric lymph pathway is involved in intestinal I/R injury and whether somatostatin (SST) affects mesenteric lymph pathway after mesenteric reperfusion. Intestinal I/R rats were treated with SST-14 by intravenous injection combined with intraperitoneal injection before occlusion of the SMA until the end of the experiment. When intestinal I/R injury treated with SST, the volumes of mesenteric lymph flow at the 6th h after reperfusion following intestinal ischemia were increased ([0.55±0.24] ml/h vs [0.25±0.09] ml/h, p<0.05) and the number of intestinal lymphocytes per milliliter ([2.30±0.72]×107/ml vs [1.16±0.63]×107/ml, p<0.05) was also increased, which caused the number of intestinal lymphocytes output at the same period of time was significantly increased compared with intestinal I/R group ([1.33±0.88]×107/h vs [0.28±0.15]×107/h, p<0.05). Meanwhile, the number of 51Cr-lymphocytes migration from systemic circulation to the effector sites in GALT was significantly increased ([1.93±0.23]×105/h vs [0.90±0.25]×105/h, p<0.05), although the percentage of 51Cr-lymphocytes in the effector sites ([1.45±0.26]% vs [3.23±1.69]%, p<0.05) was sharply decreased compared with intestinal I/R group. The accompanying decreases of the endotoxin concentration ([0.038±0.017] EU/mL vs [0.110±0.028] EU/mL, compared with intestinal I/R group p<0.05) and the TNF-α levels ([37.50±10.45] ρg/ml) vs ([74.93±14.77] ρg/ml), compared with intestinal I/R group p<0.05) in mesenteric lymph and the improvement of vital organ dysfunction happened during the early intestinal I/R injury. Suppression of gut-derived toxic mediators reaching systemic circulation and increases of the number of lymphocytes homing to the effector sites in GALT to strengthen the effective immune responses in intestinal mucosa account for the protective effects of exogenous SST against early intestinal I/R injury.

Intravenous catecholamine administration affects mouse intestinal lymphocyte number and apoptosis

The purposes of this study were to determine plasma and intestinal epinephrine (E) and norepinephrine (NE) concentrations in mice after exercise stress and, the effect of intravenous injection of E and NE (at concentrations during exercise) on viability of intestinal lymphocytes (IL). Exhaustive exercise significantly elevated plasma E and NE, and intestinal E, compared with sedentary animals. Twenty-four hours after intravenous NE administration, IL counts were higher (p<0.001) and % apoptotic IL were lower ( p<0.001) than saline conditions. E resulted in fewer apoptotic IL at 24 h compared to saline controls. E and NE differentially influence IL numbers at 24 h after injection although both result in fewer % apoptotic IL relative to mice given saline only.

Intestinal lymphocyte number, migration and antibody secretion in young and old rats.

This study demonstrates that the mucosal immune response to cholera toxin (CT) is compromised in old rats in comparison with young animals. The total number of immunoglobulin A (IgA)-secreting cells is similar or higher in the intestinal inductor and effector sites in old animals. However, the number of specifically induced anti-CT IgA antibody-secreting cells is lower in these tissues in comparison with those in young animals. The kinetics of this immune response in the different gut-associated lymphoid tissues studied suggests that the age-associated decline in the number of anti-CT IgA-secreting cells in the intestinal mucosa reflects impaired IgA immunoblast migration. Our data from lymphocyte adoptive transfer studies indicate that factors intrinsic to both the donor cells and the host recipient influence the migration of immunoblasts from the Peyer's patches to the effector site. For example, donor cells from old donors transferred to either young or old recipient rats migrate slower than young donor lymphocytes transferred into old host animals. In vitro studies clearly indicate that ageing does not impair antibody secretion by intestinal mucosal plasma cells. Therefore, the age-related decline in the intestinal mucosal immune response, e.g. diminished specific antibody titres in intestinal lavage, reflects fewer antibody-secreting cells in the mucosa.

Intestinal immune function is unaffected by parenteral nutrition in man.

Animal studies have demonstrated intestinal immunoglobulin production is decreased when luminal nutrition is withheld and nutrition is provided solely on the basis of total parenteral nutrition (TPN). Eight normal volunteers were hospitalized in the Clinical Research Center for three weeks. The subjects received TPN as an exclusive means of nutritional support for 14 days followed by 5 days of enteral feeding with either standard or a glutamine- and arginine-supplemented formula in which the protein source was primarily free amino acids and peptides. Endoscopic jejunal biopsies obtained before and after TPN and following enteral refeeding were evaluated by immunofluorescence for the number of IgA, IgM and IgG-producing cells; T and B cells as well as intraepithelial and lamina propria lymphocytes were also counted. Serum immunoglobulins and the molecular forms of serum IgA were determined at the same intervals. The number of intestinal IgA-, IgM- and IgG-producing cells was unaffected by TPN (676 +/- 58 vs. 643 +/- 38, 101 +/- 14 vs. 98 +/- 18, 10 +/- 1 vs. 11 +/- 2 per low power field). The total number of intestinal lymphocytes, and CD3+ lymphocytes in the intraepithelial area was unaffected by TPN (10.4 +/- 0.4 vs. 10.2 +/- 1.3, 7.3 +/- 0.8 vs. 8.6 +/- 1.6 per 100 epithelial cells). Similarly, the total number of lymphocytes and CD3+ lymphocytes in the intestinal lamina propria was unaffected by TPN (4.4 +/- 0.2 vs. 6.2 +/- 0.8, 3.3 +/- 0.7 vs. 4.5 +/- 0.8). A small, but statistically significant increase in serum IgA and IgM was seen with TPN 314 +/- 11 vs. 342 +/- 16 mg/dL and 154 +/- 25 vs. 226 +/- 47 mg/dL, although IgG remained unchanged (1262 +/- 69 vs. 1207 +/- 57 mg/dL). The proportion of polymeric and monomeric serum IgA remained unchanged after TPN (19.2 vs. 22.1% polymeric). The use of TPN is not associated with intestinal immune dysfunction in man. A small, but statistically significant increase in serum IgM, and a borderline statistically significant increase in serum IgM were associated with TPN. The etiology and clinical significance of these observations is unclear.

Resistance to intestinal parasites during murine AIDS: role of alcohol and nutrition in immune dysfunction.

A murine AIDS model with many similarities to human AIDS, LP-BM5 Murine Leukaemia, suppresses T and B cell numbers and functions in the intestine. This permits chronic colonization by Giardia and Cryptosporidium. Cocaine and the nutrient alcohol, which are immunosuppressive, further reduce resistance to intestinal parasites and intestinal lymphocyte numbers. Protein undernutrition, vitamin E supplementation, and alcohol use further modify immune dysfunction induced by the murine retrovirus infection. This suggests that both undernutrition and nutrient supplementation could affect parasite resistance during AIDS. Thus this murine model of human AIDS has great potential to accelerate studies of the role of nutrients in immune dysfunction and resistance to intestinal parasites.