Pulmonary-intestinal cross-talk in mucosal inflammatory disease.

Mycobacterium avium subspecies paratuberculosis (MAP) is a member of the M avium complex (MAC) It differs genetically from other MAC in having 14 to 18 copies of IS900 and a single cassette of DNA involved in the biosynthesis of surface carbohydrate Unlike other MAC, MAP is a specific cause of chronic inflammation of the intestine in many animal species, including primates The disease ranges from pluribacillary to paucimicrobial, with chronic granulomatous inflammation like leprosy in humans MAP infection can persist for years without causing clinical disease The herd prevalence of MAP infection in Western Europe and North America is reported in the range 21% to 54% These subclinically infected animals shed MAP in their milk and onto pastures MAP is more robust than tuberculosis, and the risk that is conveyed to human populations in retail milk and in domestic water supplies is high MAP is harboured in the ileocolonic mucosa of a proportion of normal people and can be detected in a high proportion of full thickness samples of inflamed Crohn's disease gut by improved culture systems and IS900 polymerase chain reaction if the correct methods are used MAP in Crohn's disease is present in a protease-resistant nonbacillary form, can evade immune recognition and probably causes an immune dysregulation As with other MAC, MAP is resistant to most standard antituberculous drugs Treatment of Crohn's disease with combinations of drugs more active against MAC such as rifabutin and clarithromycin can bring about a profound improvement and, in a few cases, apparent disease eradication New drugs as well as effective MAP vaccines for animals and humans are needed The problems caused by MAP constitute a public health issue of tragic proportions for which a range of remedial measures are urgently needed

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Causation of Crohn's disease by Mycobacterium avium subspecies paratuberculosis

https://www.amjmed.com/article/0002-9343(90)90425-D/pdf

Evaluation and management of scleroderma lung disease using bronchoalveolar lavage

https://journal.chestnet.org/article/S0012-3692(15)48340-0/pdf

Thoracic manifestations of inflammatory bowel disease.

Extraintestinal manifestations of both Crohn's disease and ulcerative colitis (UC) have been well described, although pulmonary findings are often overlooked. We summarize the experience of more than 400 cases of pulmonary manifestations of inflammatory bowel disease (IBD). These manifestations will be categorized by disease mechanism into drug-induced disease, anatomic disease, over-lap syndromes, autoimmune disease, physiologic consequences of IBD, pulmonary function test abnormalities, and nonspecific lung disease. We intend to provide the clinician with a practical working update on the spectrum of pulmonary dysfunction associated with IBD.

Pulmonary manifestations of inflammatory bowel disease

We have investigated the following pulmonary related parameters in 22 patients with Crohn's disease who were free of clinical pulmonary symptoms and had normal chest roentgenograms and in 25 controls: serum angiotensin converting enzyme, pulmonary function tests, bronchoalveolar lavage (lymphocyte count and subpopulations, macrophage viability and superoxide anion release by macrophages) and pulmonary scannings. Serum angiotensin converting enzyme was lower in Crohn's disease (14.1 +/- 5.1) than in controls (25.2 +/- 4.7) (p less than 0.001). Twelve of 22 Crohn's disease (54%) had a bronchoalveolar lavage lymphocytosis (greater than 18% alveolar lymphocytes). Bronchoalveolar lavage lymphocytes subpopulations were quite variable. Twelve of 17 Crohn's disease (71%) had an increase spontaneous and/or stimulated superoxide anion production by alveolar macrophages. Six of 12 Crohn's disease (50%) had an increase physiologic dead space in the upper part of their lung against one of 11 controls (9%). These data suggest that most patients with Crohn's disease have a latent pulmonary involvement.

https://gut.bmj.com/content/gutjnl/27/8/919.full.pdf

Latent pulmonary involvement in Crohn's disease: biological, functional, bronchoalveolar lavage and scintigraphic studies.

A study was initiated to determine whether alveolar macrophages from patients with collagen vascular diseases but free of pulmonary symptoms were spontaneously activated and whether they released various mediators related to the pathogenesis of pulmonary fibrosis. Alveolar macrophages obtained by bronchoalveolar lavage from 32 patients with proved collagen vascular disease but no evidence of lung disease were compared with those from 10 patients with collagen vascular disease with interstitial lung disease (CVD-ILD) and from 10 healthy controls. The total number of alveolar macrophages did not differ between patients with collagen vascular disease and controls but were substantially increased in the CVD-ILD group. Alveolar macrophages from 31 of the 32 patients with collagen vascular disease and from all 10 in the CVD-ILD group had at least one criterion of activation. Neutrophil chemotactic activity was detected in supernatants from alveolar macrophage culture in 23 of the 32 patients with collagen vascular disease and from nine of the 10 in the CVD-ILD group; fibronectin secretion by alveolar macrophages was increased in 12 of the 32 patients with collagen vascular disease and in nine of the 10 in the CVD-ILD group. Furthermore, alveolar macrophages from 20 of the 32 patients with collagen vascular disease and four of the 10 CVD-ILD patients spontaneously released increased amounts of superoxide anion. Thus alveolar macrophages were spontaneously activated in a high proportion of patients with collagen vascular disease.

https://thorax.bmj.com/content/thoraxjnl/43/1/24.full.pdf

C. Voisin

Papers

Latent pulmonary involvement in Crohn's disease: biological, functional, bronchoalveolar lavage and scintigraphic studies.

Activated alveolar macrophages in subclinical pulmonary inflammation in collagen vascular diseases.

Insulin in the Somogyi Phenomenon