Germ free animal studies show that beings lacking a microbiome have underdeveloped immune systems (7). Germ free animals have noticeable defects in their spleen, thymus, lymph nodes, and other lymphoid tissues (1). The introduction of commensal microorganisms have shown increased helper T cell levels, induced immunoglobulin A antibody production, and development of organized lymphoid tissues of previously uncolonized organisms (7).The balance of helper T cell subsets (TH1 and TH2) can be restored to near normal levels when germ free mice are colonized with bacteria containing polysaccharide A (PSA) (2). Some germ free mice have impaired innate lymphoid cells, which are lymphoid cells that lack both a B and T cell receptor, and therefore have decreased levels of interleukin 22 (IL-22), which is a critical cytokine during the opsonization of microbes in the small intestine (1). Under germ free conditions there are also reductions in the levels of helper T cells in the small intestine (8). Although not much is known about how commensal bacteria effect host immunity, there are specifc microorganisms, like Bacteroides fragilis, that are known to be potent immune modulators (7). Colonizing germ free mice with species like Bacteroides fragilis has been shown to restore TH17 cell levels to that of animals with standard microbial colonization (9). There are, however, studies that show germ free mice that were colonized with microbes later in life have different adult transcriptional profiles than mice missing only one specific pathogen (1). This suggests that if microbial colonization does not occur during a specific early-life time frame, the implications to immune development may be irreversible and may lead to an adult immune system that is not fully functional, or even potentially
Germ free animal studies show that beings lacking a microbiome have underdeveloped immune systems (7). Germ free animals have noticeable defects in their spleen, thymus, lymph nodes, and other lymphoid tissues (1). The introduction of commensal microorganisms have shown increased helper T cell levels, induced immunoglobulin A antibody production, and development of organized lymphoid tissues of previously uncolonized organisms (7).The balance of helper T cell subsets (TH1 and TH2) can be restored to near normal levels when germ free mice are colonized with bacteria containing polysaccharide A (PSA) (2). Some germ free mice have impaired innate lymphoid cells, which are lymphoid cells that lack both a B and T cell receptor, and therefore have decreased levels of interleukin 22 (IL-22), which is a critical cytokine during the opsonization of microbes in the small intestine (1). Under germ free conditions there are also reductions in the levels of helper T cells in the small intestine (8). Although not much is known about how commensal bacteria effect host immunity, there are specifc microorganisms, like Bacteroides fragilis, that are known to be potent immune modulators (7). Colonizing germ free mice with species like Bacteroides fragilis has been shown to restore TH17 cell levels to that of animals with standard microbial colonization (9). There are, however, studies that show germ free mice that were colonized with microbes later in life have different adult transcriptional profiles than mice missing only one specific pathogen (1). This suggests that if microbial colonization does not occur during a specific early-life time frame, the implications to immune development may be irreversible and may lead to an adult immune system that is not fully functional, or even potentially