A novel IL-17-dependent mechanism of cross protection: respiratory infection with mycoplasma protects against a secondary listeria infection.
Immune responses to pathogens occur within the context of current and previous infections. Cross protection refers to the phenomena where infection with a particular pathogen provides enhanced resistance to a subsequent unrelated pathogen in an antigen-independent manner. Proposed mechanisms of antigen-independent cross protection have involved the secretion of IFN-gamma, which activates macrophages, thus providing enhanced innate immunity against the secondary viral or bacterial pathogen. Here we provide evidence that a primary infection with the chronic respiratory pathogen, Mycoplasma pulmonis, provides a novel form of cross protection against a secondary infection with Listeria monocytogenes that is not mediated by IFN-gamma, but instead relies upon IL-17 and mobilization of neutrophils. Mice infected with M. pulmonis have enhanced clearance of L. monocytogenes from the spleen and liver, which is associated with increased numbers of Gr-1(+)CD11b(+) cells and higher levels of IL-17. This enhanced clearance of L. monocytogenes was absent in mice depleted of Gr-1(+) cells or in mice deficient in the IL-17 receptor. Additionally, both the IL-17 receptor and neutrophils were essential for optimal clearance of M. pulmonis. Thus, a natural component of the immune response directed against M. pulmonis was able to enhance clearance of L. monocytogenes.
Sieve
Amy N
AN
Department of Molecular Biology and Immunology, The University of North Texas Health Science Center, Fort Worth, TX, USA.
Meeks
Karen D
KD
Bodhankar
Sheetal
S
Lee
Suheung
S
Kolls
Jay K
JK
Simecka
Jerry W
JW
Berg
Rance E
RE
D000818:Animals; D005260:Female; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D008089:Listeria monocytogenes / Q000276:immunology*; D008088:Listeriosis / Q000276:immunology* / Q000382:microbiology; D008099:Liver / Q000276:immunology / Q000382:microbiology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009175:Mycoplasma Infections / Q000276:immunology* / Q000382:microbiology; D045803:Mycoplasma pulmonis / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D053722:Receptors, Interleukin-17 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D013154:Spleen / Q000276:immunology / Q000382:microbiology
D020381:Interleukin-17; D053722:Receptors, Interleukin-17; D007371:Interferon-gamma