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PLoS One. 2017 Jul 10;12(7):e0180212. doi: 10.1371/journal.pone.0180212. eCollection 2017.

Effects of clinical and environmental factors on bronchoalveolar antibody responses to Pneumocystis jirovecii: A prospective cohort study of HIV+ patients.

Author information

1
Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, California, United States of America.
2
Division of Pediatric Pulmonology, University of California, San Francisco, California, United States of America.
3
Division of Infectious Diseases, University of Cincinnati, Cincinnati, Ohio, United States of America.
4
Veterans Administration Medical Center, Cincinnati, Ohio, United States of America.
5
HIV/AIDS Division, San Francisco General Hospital, University of California, San Francisco, California, United States of America.
6
Environmental Health Sciences, University of California, Berkeley, California, United States of America.
7
Research Department of Infection and Population Health, Institute of Epidemiology and Healthcare, University College London, London, United Kingdom.
8
Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom.

Abstract

BACKGROUND:

Humoral immunity plays an important role against Pneumocystis jirovecii infection, yet clinical and environmental factors that impact bronchoalveolar antibody responses to P. jirovecii remain uncertain.

METHODS:

From October 2008-December 2011 we enrolled consecutive HIV-infected adults admitted to San Francisco General Hospital (SFGH) who underwent bronchoscopy for suspected Pneumocystis pneumonia (PCP). We used local air quality monitoring data to assign ozone, nitrogen dioxide, and fine particulate matter exposures within 14 days prior to hospital admission. We quantified serum and bronchoalveolar lavage fluid (BALF) antibody responses to P. jirovecii major surface glycoprotein (Msg) recombinant constructs using ELISA. We then fit linear regression models to determine whether PCP and ambient air pollutants were associated with bronchoalveolar antibody responses to Msg.

RESULTS:

Of 81 HIV-infected patients enrolled, 47 (58%) were diagnosed with current PCP and 9 (11%) had a prior history of PCP. The median CD4+ count was 51 cells/μl (IQR 15-129) and 44% were current smokers. Serum antibody responses to Msg were statistically significantly predictive of BALF antibody responses, with the exception of IgG responses to MsgC8 and MsgC9. Prior PCP was associated with increased BALF IgA responses to Msg and current PCP was associated with decreased IgA responses. For instance, among patients without current PCP, those with prior PCP had a median 73.2 U (IQR 19.2-169) IgA response to MsgC1 compared to a 5.00 U (3.52-12.6) response among those without prior PCP. Additionally, current PCP predicted a 22.5 U (95%CI -39.2, -5.82) lower IgA response to MsgC1. Ambient ozone within the two weeks prior to hospital admission was associated with decreased BALF IgA responses to Msg while nitrogen dioxide was associated with increased IgA responses.

CONCLUSIONS:

PCP and ambient air pollutants were associated with BALF IgA responses to P. jirovecii in HIV-infected patients evaluated for suspected PCP.

PMID:
28692651
PMCID:
PMC5503245
DOI:
10.1371/journal.pone.0180212
[Indexed for MEDLINE]
Free PMC Article

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