Abstract
Mastitis, inflammation of the mammary gland, is a common disease of dairy animals. The disease is caused by bacterial infection ascending through the teat canal and mammary pathogenic Escherichia coli (MPEC) are common etiology. In the first phase of infection, virulence mechanisms, designated as niche factors, enable MPEC bacteria to resist innate antimicrobial mechanisms, replicate in milk, and to colonize the mammary gland. Next, massive replication of colonizing bacteria culminates in a large biomass of microbe-associated molecular patterns (MAMPs) recognized by pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) mediating inflammatory signaling in mammary alveolar epithelial cells (MAEs) and macrophages. Bacterial lipopolysaccharides (LPSs), the prototypical class of MAMPs are sufficient to elicit mammary inflammation mediated by TLR4 signaling and activation of nuclear factor kB (NF-kB), the master regulator of inflammation. Using in vivo mastitis model, in low and high complements mice, and in vitro NF-kB luminescence reporter system in MAEs, we have found that the smooth configuration of LPS O-polysaccharides in MPEC enables the colonizing organisms to evade the host immune response by reducing inflammatory response and conferring resistance to complement. Screening a collection of MPEC field strains, we also found that all strains were complement resistant and 94% (45/48) were smooth. These results indicate that the structure of LPS O-polysaccharides chain is important for the pathogenesis of MPEC mastitis and provides protection against complement-mediated killing. Furthermore, we demonstrate a role for complement, a key component of innate immunity, in host-microbe interactions of the mammary gland.
Highlights
Mastitis, inflammation of the mammary gland, is an important disease in dairy animals and Escherichia coli (E. coli) is a common etiology [1, 2]
Massive replication of colonizing bacteria culminates in a large biomass of microbial associated molecular patterns (MAMPs) recognized by pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) mediating inflammatory signaling in mammary alveolar epithelial cells (MAEs) and macrophages [1, 4]
E. coli strains causing extraintestinal infections are commonly designated as extraintestinal pathogenic E. coli (ExPEC) [50]
Summary
Inflammation of the mammary gland, is an important disease in dairy animals and Escherichia coli (E. coli) is a common etiology [1, 2]. Other virulence traits that are not related to the proinflammatory activity of LPS might be affected by the length and structure of the O-polysaccharides, most notable are resistance to complement and phagocytosis and killing by macrophages and neutrophils [10,11,12,13]. The variable structure and antigenicity of the O-polysaccharides chains have been extensively used for classical serological O-typing of many gramnegative bacteria including MPEC. Thereupon many specific O-serotypes were linked to virulence, pathotypes and clinical syndromes, most notable examples are O157 enterohemorrhagic E. coli (EHEC), O127 enteropathogenic E. coli (EPEC). This simple technique has been extensively used for decades to classify MPEC isolates, specific O-types could not be linked to mammary virulence or clinical and epidemiological characteristics of the disease. Serum resistance and smooth colony morphology have been linked to virulence in many bacterial pathogens including MPEC [8, 15]
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