Papel dos anticorpos induzidos pela microbiota na responsividade inflamatória do hospedeiro

Abstract

Nowhere in the study of human biology are basic concepts changing more rapidly than with respect to the human microbiota. The indigenous intestinal microbiota is frequently considered as an additional major organ of the human body responsible for three main functions: colonization resistance, nutritional contribution, and immune modulation. Germ-free (GF) mice are an important tool to properly assess the effects of colonization in host physiology. Recently, works form our group showed that GF mice displays a significantly different inflammatory responsiveness pattern, which was dubbed "the hyporesponsiveness phenotype". Where conventional mice succumbs to the systemic inflammatory response unleashed by the reperfusion of the ischemic superior mesenteric artery, GF mice presented little evidence of local or systemic injury after intestinal ischemia and reperfusion. The inability of germfree mice to inflame in response to systemic LPS or reperfusion-induced injury was largely because of the innate capacity of these mice to produce IL-10 and, possibly, other anti-inflammatory molecules. The deposition of immune complexes is a major event in acute systemic inflammation. GF mice have a distinct difference in their immunoglobulin (Ig) repertoire and B cell activity. Our goal in the present work was to evaluate the role of the immunoglobulin repertoire in the inflammatory hyporesponsiveness in GF mice. We found that the serum and Ig transfer from CV mice was capable to revert the inflammatory responsiveness of GF mice both in a sterile systemic inflammatory injury as in lung infection by K. pneumonia. Thus, our data shows that the serum and Ig transfer from CV mice promotes the reestablishment of conventional inflammation in GF mice.