It’s not just that antibiotics don’t help a viral infection, an important paper just published in the Proceedings of the National Academy of Sciences (USA) demonstrates that they impair the immune response to the flu. The authors state:
“Although commensal bacteria are crucial in maintaining immune homeostasis of the intestine, the role of commensal bacteria in immune responses at other mucosal surfaces remains less clear. Here, we show that commensal microbiota composition critically regulates the generation of virus-specific CD4 and CD8 T cells and antibody responses following respiratory influenza virus infection.”
They investigated various antibiotic treatments and found that neomycin-sensitive bacteria required to produce protective immune responses in the lung.
“Intact microbiota provided signals leading to the expression of mRNA for pro–IL-1β and pro–IL-18 at steady state. Following influenza virus infection, inflammasome activation led to migration of dendritic cells (DCs) from the lung to the draining lymph node and T-cell priming.”
In other words, the normal bacterial residing in the intestines (that are wiped out by common antibiotics) play a critical role in the cellular signaling necessary to mount an immune antiviral response. The authors conclude:
“Our results reveal the importance of commensal microbiota in regulating immunity in the respiratory mucosa through the proper activation of inflammasomes.”
An ‘editor’s choice’ essay published in Science Signaling commenting on this important study observes:
“Both virion-specific antibody titers and T cell responses (interferon-{gamma} production and number of cytotoxic T cells) were decreased in antibiotic-treated mice compared with untreated controls, and pulmonary viral titers were increased…The adaptive immune response to respiratory infection with influenza depends on activation of inflammasomes…such as interleukin-1β (IL-1β) and IL-18…Antibiotic treatment decreased the abundance of the mRNAs encoding pro–IL-1β, pro–IL-18, and NLRP3 even before infection, as well as postinfection secretion of mature IL-1β, suggesting that commensal bacteria provide a constitutive priming signal. Antibiotics also inhibited migration of respiratory dendritic cells to lymph nodes to activate T cells…Thus, the authors propose that commensal bacteria provide a signal required for inflammasome-dependent immune responses to respiratory infection, which is lost with antibiotic-mediated disruption of the microbiota.”
Bottom line: wiping out commensal bacterial with antibiotics hobbles the immune response to viral respiratory infection.
