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Expression of secretory leukocyte proteinase inhibitor in the submandibular glands of AIDS patients
Author(s) -
Rocha LA,
Vargas PA,
Silva LFF,
Leon JE,
Santos AB,
Hiemstra PS,
Mauad T
Publication year - 2008
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2006.01358.x
Subject(s) - slpi , betaherpesvirinae , sialadenitis , protease inhibitor (pharmacology) , submandibular gland , human cytomegalovirus , immunohistochemistry , cytomegalovirus , immunology , biology , proteinase 3 , pathology , medicine , virus , viral disease , herpesviridae , salivary gland , viral load , inflammation , antiretroviral therapy , myeloperoxidase
Objective:  Secretory leukocyte proteinase inhibitor (SLPI) is an endogenous proteinase inhibitor present in mucosal secretions. It also displays antimicrobial activity including anti‐human immunodeficiency virus activity. This protease inhibitor is also expressed in submandibular glands (SMG), but there are few data on its expression in AIDS patients with infectious conditions. Methods:  We analyzed the expression of SLPI using immunohistochemistry in submandibular gland samples of 36 AIDS patients [10 with normal histology, 10 with chronic nonspecific sialadenitis, eight with mycobacteriosis, and eight with cytomegalovirus (CMV) infection] and 10 HIV‐negative controls. The proteinase inhibitor was quantified using image analysis and expressed as % of positively stained area. Results:  There was a higher expression of SLPI in AIDS patients with CMV infection (% of stained area, mean ± SD: 37.37 ± 14.45) when compared with all other groups ( P  = 0.009). There were no significant differences between control subjects (22.70 ± 9.42%) and AIDS patients without histologic alterations (18.10 ± 7.58%), with chronic nonspecific sialadenitis (17.13 ± 5.36%), or mycobacterial infection (21.09 ± 4.66%). Conclusion:  Cytomegalovirus infection increases SLPI expression in the SMG of AIDS patients. Our results reveal new insights into the pathogenic association between HIV and CMV in AIDS patients.

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