title: Chronic helminth infection does not exacerbate Mycobacterium tuberculosis infection.
abstract: BACKGROUND
  Chronic helminth infections induce a Th2 immune shift and establish an immunoregulatory milieu. As both of these responses can suppress Th1 immunity, which is necessary for control of Mycobacterium tuberculosis (MTB) infection, we hypothesized that chronic helminth infections may exacerbate the course of MTB.
  
  
  RESULTS
  Co-infection studies were conducted in cotton rats as they are the natural host for the filarial nematode Litomosoides sigmodontis and are an excellent model for human MTB. Immunogical responses, histological studies, and quantitative mycobacterial cultures were assessed two months after MTB challenge in cotton rats with and without chronic L. sigmodontis infection. Spleen cell proliferation and interferon gamma production in response to purified protein derivative were similar between co-infected and MTB-only infected animals. In contrast to our hypothesis, MTB loads and occurrence and size of lung granulomas were not increased in co-infected animals.
  
  
  CONCLUSIONS
  These findings suggest that chronic filaria infections do not exacerbate MTB infection in the cotton rat model. While these results suggest that filaria eradication programs may not facilitate MTB control, they indicate that it may be possible to develop worm-derived therapies for autoimmune diseases that do not substantially increase the risk for infections.
authors.affiliation: Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, United States of America. huebner@microbiology-bonn.de
authors.forename: Marc P
authors.initials: MP
authors.lastname: Hübner
authors.forename: Kristin E
authors.initials: KE
authors.lastname: Killoran
authors.forename: Michael
authors.initials: M
authors.lastname: Rajnik
authors.forename: Samuel
authors.initials: S
authors.lastname: Wilson
authors.forename: Kevin C
authors.initials: KC
authors.lastname: Yim
authors.forename: Marina N
authors.initials: MN
authors.lastname: Torrero
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Morris
authors.forename: Boris
authors.initials: B
authors.lastname: Nikonenko
authors.forename: Jorge C G
authors.initials: JC
authors.lastname: Blanco
authors.forename: Val G
authors.initials: VG
authors.lastname: Hemming
authors.forename: Edward
authors.initials: E
authors.lastname: Mitre
mesh_terms: D000818:Animals; D058491:Bacterial Load; D049109:Cell Proliferation; D002908:Chronic Disease; D060085:Coinfection / Q000276:immunology / Q000382:microbiology / Q000469:parasitology / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D005368:Filariasis / Q000150:complications* / Q000276:immunology; D005370:Filarioidea / Q000276:immunology / Q000472:pathogenicity; D006651:Histocytochemistry; D007371:Interferon-gamma / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008168:Lung / Q000382:microbiology / Q000473:pathology; D009169:Mycobacterium tuberculosis / Q000276:immunology / Q000472:pathogenicity; D016205:Sigmodontinae; D013154:Spleen / Q000276:immunology; D014376:Tuberculosis / Q000150:complications* / Q000276:immunology / Q000473:pathology*
chemical_list: D007371:Interferon-gamma