Impact of streptococcus pneumoniae bacteremia and human immunodeficiency virus type 1 on oral mucosal immunity

Nancy L. Opstad, Charles L. Daley, Joseph R Thurn, Jeff B Rubins, Cindy Merrifield, Philip C. Hopewell, Edward N. Janoff

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

To determine whether defects in mucosal immunity were associated with invasive disease caused by a mucosal pathogen, Streptococcus pneumoniae, levels of salivary immunoglobulins and nonspecific immune factors were compared in subjects with human immunodeficiency virus type 1 (HIV-1) infection and in HIV-1-seronegative subjects with and without pneumococcal bacteremia. The IgA2 subclass may be of particular importance because S. pneumoniae produces IgA1 protease, which cleaves IgA1 but not IgA2. Levels (37-56 μg/mL) and proportions (11%-17%) of IgA2 were similar among groups. Serotype-specific capsular salivary 19A was present in a minority of patients with acute bacteremia. Levels of lactoferrin were increased with bacteremia. Neither selective mucosal IgA2 deficiency nor impaired nonspecific upper respiratory mucosal responses were associated with invasive pneumococcal disease during HIV-1 infection; thus, other defects in mucosal cellular responses and systemic immunity may predispose HIV-1-infected patients to invasive pneumococcal disease.

Original languageEnglish (US)
Pages (from-to)566-570
Number of pages5
JournalJournal of Infectious Diseases
Volume172
Issue number2
DOIs
StatePublished - Aug 1995

Bibliographical note

Funding Information:
Received 23 January 1995; revised 30 March 1995. Presented in part: 34th Interscience Conference on Antimicrobial Agents and Chemotherapy, Orlando, Florida, 4 October 1994. Written informed consent was obtained from each subject for protocols approved by the University of California at San Francisco and San Francisco General Hospital and the Minneapolis VA Medical Center. Financial support: National Institutes of Health (AI-31373, DE-42600), Department ofVeterans Affairs Research Service, and Minnesota Medical Foundation. Reprints or correspondence: Dr. Edward N. Janoff, VA Medical Center, Infectious Disease Section (151), One Veterans Dr., Minneapolis, MN 55417.

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