Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery.

Williams, Andrew E.; Heath, Donald; Kày, J. M.; Smith, Paul

doi:10.1136/thx.32.3.287

Cited by 22 publications

(16 citation statements)

References 29 publications

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“…Previously, we [2][3][4]17] and others [18][19][20][21][22][23] have found that mast cell and goblet cell numbers increase as responses to noxious and immunological stimuli. The increased numbers of activated lymphoid cells noted in capsaicin-treated animals, if releasing cell growth factors, may consequently be responsible for the increased numbers of mast cells and goblet cells seen in the present study.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of the Bronchial Reactivity in Immunized Rats by Neonatal Treatment with Capsaicin

Ahlstedt¹,

Alving²,

Hesselmar

et al. 1986

Int Arch Allergy Immunol

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Rats were injected with capsaicin at 1–2 days of age to abolish the content of substance P (SP) in nerve terminals. At 6 weeks of age the capsaicin-treated and control rats were sensitized daily for 1 or 2 subsequent weeks Monday through Friday with ovalbumin (OA). The OA was given without adjuvant as 300 ng subcutaneous (s.c.) injections in the neck region or as 1% aerosol for 30 min. The capsaicin-treated animals which were sensitized s.c. for 2 weeks reacted moderately with increased transpulmonary pressure (TPP) to airway challenge with OA, and strongly to intravenous (i.v.) challenge with OA or serotonin. The capsaicin-untreated animals, which were sensitized with OA, reacted weakly to the challenge. In the animals sensitized with aerosolized OA, slightly lower reactivity was seen compared with those sensitized s.c. Untreated and unsensitized control rats reacted only to serotonin challenge. No animal had any detectable serum or bronchial IgE antibodies. Aerosol-sensitized animals had IgG antibodies in both serum and bronchial lavage. Histologically, the animals treated with capsaicin in contrast to the untreated controls demonstrated a pronounced increase of lymphoid tissue around their bronchi. Their mast cell numbers were increased around vessels and in the pleura and their mucous cell numbers were increased in the epithelium of the bronchi and bronchioli. The sensitization did not add much to this histological picture.

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Section: Discussionmentioning

confidence: 99%

Enhancement of the Bronchial Reactivity in Immunized Rats by Neonatal Treatment with Capsaicin

Ahlstedt¹,

Alving²,

Hesselmar

et al. 1986

Int Arch Allergy Immunol

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“…The accumulation of mono nuclear cells was decreased after such immunosup pressive treatment with intravenous PSA, whereas the development of mast cells and mucus-produc ing cells was less affected. This discrepancy might be explained by the latter cell types being more sus ceptible to immunological nonspecific irritation [8,11,12].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that local immune re sponses including DH in the lung [2] as well as cellmediated immunity in the gut [9,10] and noxious stim ulation of mucosal membranes [8,II,12] are nor mally accompanied by the appearance of increased numbers of mononuclear cells, mast cells and mucusproducing cells. This may partly be due to the produc tion of T-cell-derived lymphokines [7].…”

Section: Discussionmentioning

confidence: 99%

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Immunological Suppression of Delayed Hypersensitivity Responses in Mouse Lungs as Reflected by Numbers of Mononuclear Cells, Mast Cells and Mucus-Producing Cells

Enander¹,

Nygren

Ahlstedt

1988

Int Arch Allergy Immunol

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The suppression of delayed hypersensitivity (DH) in the lung as reflected by the appearance of mononuclear cells, mast cells and mucus-producing cells was studied in Balb/c mice. Immunosuppression was induced by intravenous and peroral administration of picrylsulfonic acid (PSA) in mice subsequently sensitized with picrylchloride (PiCl). The animals exhibited a decreased DH reactivity as assessed by ear thickness increase compared with mice sensitized but not exposed to PSA pretreatment. In mice exposed to PSA intravenously (suppressed) and sensitized with PiCl there was a decrease in the number of mononuclear cells in the lung after challenge, compared to mice sensitized and challenged only. Similarly, the mast cell and mucus-producing cell numbers were slightly lower in animals immunosuppressed intravenously with PSA compared with sensitized mice. Such a decrease in the numbers of mononuclear cells, mast cells and mucus-producing cells in the lung was not seen in animals treated with PSA perorally, although these animals exhibited suppressed DH reaction in the ears. The present results indicate that induction of mononuclear cells and to some extent mast cells and mucus-producing cells in the lung relates to the DH reaction and its regulation.

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“…In contrast, adult rats maintained at a barometric pressure of 380 mm Hg for 35 days exhibit a proliferation of mast cells around pulmonary blood vessels and in alveolar septa. There is a correlation between perivascular lung mast cell density and medial thickness of muscular pulmonary arteries [104]. The MMP family of proteolytic enzymes is involved in remodeling of the extracellular matrix.…”

Section: Activated Systemic Inflammation Is Critical For the Progressmentioning

confidence: 99%

Alveolar Hypoxia-Induced Pulmonary Inflammation: From Local Initiation to Secondary Promotion by Activated Systemic Inflammation

Chen¹,

Yang²,

Li³

et al. 2016

J Vasc Res

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Pulmonary hypertension (PH) is a pathological condition with high mortality and morbidity. Hypoxic PH (HPH) is a common form of PH occurring mainly due to lung disease and/or hypoxia. Most causes of HPH are associated with persistent or intermittent alveolar hypoxia, including exposure to high altitude and chronic obstructive respiratory disease. Recent evidence suggests that inflammation is a critical step for HPH initiation and development. A detailed understanding of the initiation and progression of pulmonary inflammation would help in exploring potential clinical treatments for HPH. In this review, the mechanism for alveolar hypoxia-induced local lung inflammation and its progression are discussed as follows: (1) low alveolar PO₂ levels activate resident lung cells, mainly the alveolar macrophages, which initiate pulmonary inflammation; (2) systemic inflammation is induced by alveolar hypoxia through alveolar macrophage activation; (3) monocytes are recruited into the pulmonary circulation by alveolar hypoxia-induced macrophage activation, which then contributes to the progression of pulmonary inflammation during the chronic phase of alveolar hypoxia, and (4) alveolar hypoxia-induced systemic inflammation contributes to the development of HPH. We hypothesize that a combination of alveolar hypoxia-induced local lung inflammation and the initiation of systemic inflammation (“second hit”) is essential for HPH progression.

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Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery.

Cited by 22 publications

References 29 publications

Enhancement of the Bronchial Reactivity in Immunized Rats by Neonatal Treatment with Capsaicin

Enhancement of the Bronchial Reactivity in Immunized Rats by Neonatal Treatment with Capsaicin

Immunological Suppression of Delayed Hypersensitivity Responses in Mouse Lungs as Reflected by Numbers of Mononuclear Cells, Mast Cells and Mucus-Producing Cells

Alveolar Hypoxia-Induced Pulmonary Inflammation: From Local Initiation to Secondary Promotion by Activated Systemic Inflammation

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