IMMUNOHISTOCHEMICAL STUDY OF TUMOR NECROSIS FACTOR-<i>α</i>, MATRIX METALLOPROTEINASE-12, AND TISSUE INHIBITOR OF METALLOPROTEINASE-2 ON ALVEOLAR MACROPHAGES OF BALB/c MICE EXPOSED TO SHORT-TERM CIGARETTE SMOKE

Hora, Katia da; Pôrto, Luís Cristóvão

doi:10.1080/01902140500324828

Cited by 25 publications

(15 citation statements)

References 22 publications

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“…In the CS10, CS20, CS30 and CS60 groups, the II for TNF-α was significantly higher than in the control group. This finding corroborates those of previous studies, (12,16,17,25) which showed a special participation of TNF-α in emphysema induced by cigarette smoke. The II for IL-6 increased progressively in direct relation to increases in the duration of exposure.…”

Section: Discussionsupporting

confidence: 83%

“…(7,(16)(17)(18) In brief, animals in each study group were placed in the inhalation chamber (40 cm in length, 30 cm in width and…”

Section: Methodsmentioning

confidence: 99%

“…The immunohistochemical analysis was carried out using the peroxidase-conjugated avidinbiotin complex method (Goat ABC staining system, Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA), as described in a previous study conducted by our group. (16) In brief, the slides were deparaffinized and rehydrated in a graded xylene-alcohol series. Antigen retrieval was performed using a solution of 1 mM EDTA in citrate buffer (pH 8.0) at high temperature in microwave oven for 5 min.…”

Section: Introductionmentioning

confidence: 99%

“…(15) Previous studies have shown that TNF-α and MMP-12 play roles in mice exposed to cigarette smoke. (7,(16)(17)(18) The objective of the present study was to use using immunohistochemical methods in order to investigate the expression of MMP-12, TIMP-2, TNF-α and IL-6 in mice exposed to cigarette smoke.…”

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confidence: 99%

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Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Valença

Pôrto

2008

J. bras. pneumol.

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Objective: Various studies of emphysema involve long-term exposure of animals to cigarette smoke, focusing on the cell type involved in the protease/antiprotease imbalance and on extracellular matrix degradation. In emphysema, increased expression of metalloproteinases is associated with cytokines, and evidence suggests that the matrix metalloproteinase-12 (MMP-12) plays an important role. Our objective was to investigate tissue inhibitor of metalloproteinase-2 (TIMP-2), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) detection by immunohistochemical methods in mouse lung. Methods: Male C57BL/6 mice were exposed 3 times a day to the smoke of 3 cigarettes over a period of 10, 20, 30 or 60 days in an inhalation chamber (groups CS10, CS20, CS30 and CS60, respectively). Controls were exposed to the same conditions in room air. Results: A progressive increase in the number of alveolar macrophages was observed in the bronchoalveolar lavage fluid of the exposed mice. The mean linear intercept, an indicator of alveolar destruction, was greater in all exposed groups when compared to control group. In the CS10, CS20 and CS30 mice, the immunohistochemical index (II) for MMP-12 increased in parallel with a decrease in II for TIMP-2 in the CS10, CS20 and CS30 mice. The II for the cytokines TNF-α and IL-6 was greater in all exposed groups than in the control group. Emphysema, with changes in volume density of collagen and elastic fibers, was observed in the CS60 group. Conclusions: These findings suggest that cigarette smoke induces emphysema with major participation of TNF-α and IL-6 without participation of neutrophils.Keywords: Macrophages, alveolar; Emphysema; Tissue inhibitor of metalloproteinase-2; Interleukin-6. ResumoObjetivo: Muitos estudos sobre enfisema são realizados com exposição de animais à fumaça de cigarro durante um longo tempo, focando o tipo de célula envolvida no desequilíbrio protease/antiprotease e a degradação da matriz extracelular. A expressão aumentada de metaloproteinases no enfisema está associado com citocinas e evidências sugerem um papel importante da metaloproteinase de matriz-12 (MMP-12). Nosso objetivo foi estudar a detecção de inibidor tissular de metaloproteinase-2 (TIMP-2), fator de necrose tumoral alfa (TNF-α) e interleucina-6 (IL-6) por métodos imunohistoquímicos no pulmão de camundongos. Métodos: Camundongos C57BL/6 machos foram expostos 3 vezes ao dia a fumaça de 3 cigarros por um período de 10, 20, 30 ou 60 dias através de uma câmara de inalação (grupos CS10, CS20, CS30 e CS60, respectivamente). O grupo controle foi exposto às mesmas condições ao ar ambiente. Resultados: Nós observamos um aumento progressivo de macrófagos alveolares no lavado broncoalveolar dos grupos expostos. O diâmetro alveolar médio, um indicador de destruição alveolar, aumentou em todos os grupos expostos quando comparado ao grupo controle. O índice imunohistoquímico (II) para MMP-12 aumentou nos grupos CS10, CS20 e CS30 em paralelo a uma redução do II para TIMP-2 nos grupos CS10, CS20 e CS3...

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Section: Discussionsupporting

confidence: 83%

“…(7,(16)(17)(18) In brief, animals in each study group were placed in the inhalation chamber (40 cm in length, 30 cm in width and…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Valença

Pôrto

2008

J. bras. pneumol.

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“…In experimental animals, exposure to cigarette smoke consistently upregulates MMP-12 production and release [9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]; this phenomenon appears to be much more frequent than upregulation of any other MMP, although we make that statement with caution because MMP-12 has been examined much more frequently than other MMPs.…”

Section: Mmps In Emphysema: Mmp-12mentioning

confidence: 67%

Matrix metalloproteinases in COPD

Churg

Zhou²,

Wright³

2011

Eur Respir J

240

116

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There is considerable evidence that matrix metalloproteinases (MMPs) are up-and/or downregulated in chronic obstructive pulmonary disease (COPD), particularly in emphysema, in which they probably participate in proteolytic attack on the alveolar wall matrix. Recent data suggest that MMPs also have major roles in driving inflammation or shutting it down, as well as modifying the release of fibrogenic growth factors, processes that are important in the genesis of the various lesions of COPD. In cigarette smoke-induced animal models of emphysema, MMP-12 appears to play a consistent and important role, whereas the data for other MMPs are difficult to interpret. In human lungs, evidence for a role for MMPs is more tenuous and there are numerous contradictions in the literature. Little is known about the effects of MMPs in small airway remodelling, smokeinduced pulmonary hypertension and chronic bronchitis, but MMP-12 participates in experimental small airway modelling. To date, the accumulated data suggest that selective inhibition of MMP-12 might be a viable therapy for emphysema and small airway remodelling, but subtle differences in the functions of MMP-12 in animals and humans mandate caution with this approach. Whether inhibition of other MMPs might be useful is unclear.

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Prevention of lung injury by Muc1 mucin in a mouse model of repetitive Pseudomonas aeruginosa infection

et al. 2012

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Objective and design To determine whether repetitive airway Pseudomonas aeruginosa (Pa) infection results in lung inflammation and injury and, if so, whether these responses are affected by Muc1 mucin. Muc1 wild type (WT) and knockout (KO) mice were compared for body weights, lung inflammatory responses, and airspace enlargement using a chronic lung infection model system. Material Mice were treated intranasally with Pa (107 CFU) on days 0, 4, 7 and 10. On day 14, body weights, inflammatory cell numbers in bronchoalveolar lavage fluid (BALF), and airspace enlargement were measured. Differences in inflammatory responses between groups were statistically analyzed by the Student’s t test and ANOVA. Results Muc1 WT mice exhibited mild degrees of both inflammation and airspace enlargement following repetitive airway Pa infection. However, Muc1 KO mice exhibited significantly decreased body weights, greater macrophage numbers in the BALF, and increased airspace enlargement compared with Muc1 WT mice. Conclusions This is the first report demonstrating that Muc1 deficiency can lead to lung injury during chronic Pa infection in mice. These results suggest that MUC1 may play a crucial role in the resolution of inflammation during chronic respiratory infections and that MUC1 dysfunction likely contributes to the pathogenesis of chronic inflammatory respiratory disease.

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IMMUNOHISTOCHEMICAL STUDY OF TUMOR NECROSIS FACTOR-α, MATRIX METALLOPROTEINASE-12, AND TISSUE INHIBITOR OF METALLOPROTEINASE-2 ON ALVEOLAR MACROPHAGES OF BALB/c MICE EXPOSED TO SHORT-TERM CIGARETTE SMOKE

Cited by 25 publications

References 22 publications

Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro

Matrix metalloproteinases in COPD

Prevention of lung injury by Muc1 mucin in a mouse model of repetitive Pseudomonas aeruginosa infection

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