Effect of Corticosteroids on IL1β and TNFα Release by Alveolar Macrophages From Patients With AIDS and Pneumocystis carinii Pneumonia

Huang, Zheng Bo; Eden, Edward

doi:10.1378/chest.104.3.751

Cited by 46 publications

(23 citation statements)

References 22 publications

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“…The beneficial effects of CS in HIV ϩ patients with Pneumocystis pneumonia who are receiving anti-Pneumocystis drugs were thought to be due either to their anti-inflammatory properties or to their effects on the surfactant system (36). Steroids reduce cytokine production in peripheral blood, but their effects on inflammatory mediators and surfactant components in BALF have not been consistent (8,12,15,18).…”

Section: Discussionmentioning

confidence: 99%

Sensitized Splenocytes Result in Deleterious Cytokine Cascade and Hyperinflammatory Response in Rats withPneumocystisPneumonia despite the Presence of Corticosteroids

Thullen

Ashbaugh²,

Daly³

et al. 2004

Infect Immun

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The immune response to the opportunistic pulmonary pathogen Pneumocystis can have beneficial and harmful effects on the host despite the presence of corticosteroids. We hypothesized that this deleterious hyperinflammatory response is associated with exaggerated cytokine production. The adoptive transfer of at least 10 7 immune splenocytes reduced the cyst count in rats with corticosteroid-induced pneumocystosis. About 18% of these rats developed clinical illness, an increased lung weight/body weight (LW/BW) ratio, and elevated levels of interleukin 1␣ (IL-1␣), IL-1␤, IL-6, tumor necrosis factor alpha, IL-5, IL-10, and gamma interferon in the lungs. This hyperinflammatory reaction was not observed in rats that remained clinically well or in control rats. Thus, in this model, corticosteroids have little effect on the cytokine cascade or other adverse effects of the host immune response to Pneumocystis.

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Section: Discussionmentioning

confidence: 99%

Sensitized Splenocytes Result in Deleterious Cytokine Cascade and Hyperinflammatory Response in Rats withPneumocystisPneumonia despite the Presence of Corticosteroids

Thullen

Ashbaugh²,

Daly³

et al. 2004

Infect Immun

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“…In addition, patients without AIDS who develop P. carinii pneumonia frequently do so as a complication of prolonged systemic corticosteroid therapy (8). Again, although corticosteroids have profound effects on lymphocytic immunity, these agents also substantially impair macrophage activation (10,(58)(59)(60). Functional impairment in the monocyte-macrophage system has also been documented in patients with advanced malignancies (61).…”

Section: Discussionmentioning

confidence: 99%

The role of alveolar macrophages in Pneumocystis carinii degradation and clearance from the lung.

Limper¹,

Hoyte²,

Standing³

1997

J. Clin. Invest.

173

149

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Although studies indicate that alveolar macrophages participate in host defense against Pneumocystis carinii , their role in organism degradation and clearance from the lung has not yet been established. We, therefore, quantified the uptake and degradation of 35 S-labeled P. carinii by cultured macrophages, demonstrating significant degradation of P. carinii over 6 h. We further evaluated the role of macrophages in elimination of P. carinii from the living host. Rats received either intratracheal PBS, liposomal PBS (L-PBS), or liposomal dichloromethylene diphosphonate (L-Cl 2 MDP), a preparation which leads to selective depletion of macrophages. Over 72 h, L-Cl 2 MDP-treated animals had loss of Ͼ 85% of their alveolar macrophages. In contrast, L-PBS-treated rats had cellular differentials identical to rats receiving PBS. Macrophage-depleted rats and controls were next inoculated with P. carinii and organism clearance was determined after 24 h. P. carinii elimination was evaluated with both cyst counts and an ELISA directed against glycoprotein A (gpA), the major antigen of P. carinii . Both assays indicated that macrophage-depleted rats had substantial impairment of P. carinii clearance compared to L-PBS-or PBS-treated rats. These data provide the first direct evidence that macrophages mediate elimination of P. carinii from the living host. ( J. Clin. Invest. 1997. 99:2110-2117.)

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“…Several investigators indicate that glucocorticosteriods and cyclosporin A decrease proinflam matory cytokine production [33][34][35]. With regard to IL-1RA production, Santos et al [36] have reported a minimal influence of hydrocortisone on endotoxinstimulated IL-1RA production in volunteers.…”

Section: Discussionmentioning

confidence: 99%

Cytokine profiles in bronchoalveolar lavage fluid and blood in HIV‐seronegative patients with Pneumocystis carinii pneumonia

Perenboom

Schijndel

Beckers

et al. 1996

Eur J Clin Investigation

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Abstract. Concentrations and ex vivo production of interleukin-(IL-1 /?), tumour necrosis factor-a (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1RA) and TNF soluble receptors were followed in bronchoalveolar lavage (BAL) fluid and blood from 10 HIV -seronegative patients with Pneumocystis carinii pneumonia (PCP) and compared with values found in healthy volunteers. During the acute phase of PCP, TNF but not IL-6 or IL-1/? was detectable in BAL fluid. At that time, plasma concentrations of the proinfiammatory cyto kines were low, whereas plasma concentrations of the anti-inflammatory cytokines were high. The ex vivo production capacity of proinfiammatory cytokines was suppressed in the acute phase, in the blood as well as at the site of infection. During convalescence the production capacity of the blood cells normalized. The I.L-1RA production capacity of the alveolar cells was also suppressed in the acute phase, but preserved in blood cells.

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Effect of Corticosteroids on IL1β and TNFα Release by Alveolar Macrophages From Patients With AIDS and Pneumocystis carinii Pneumonia

Cited by 46 publications

References 22 publications

Sensitized Splenocytes Result in Deleterious Cytokine Cascade and Hyperinflammatory Response in Rats withPneumocystisPneumonia despite the Presence of Corticosteroids

Sensitized Splenocytes Result in Deleterious Cytokine Cascade and Hyperinflammatory Response in Rats withPneumocystisPneumonia despite the Presence of Corticosteroids

The role of alveolar macrophages in Pneumocystis carinii degradation and clearance from the lung.

Cytokine profiles in bronchoalveolar lavage fluid and blood in HIV‐seronegative patients with Pneumocystis carinii pneumonia

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