Lymphocyte responses to phytohaemagglutinin in patients with asbestosis and pleural mesothelioma

Our plain-English summary of Lymphocyte responses to phytohaemagglutinin in patients with asbestosis and pleural mesothelioma, by P.L. Haslam, A. Lukoszek, J.A. Merchant, et al (Clinical and Experimental Immunology, 1978).

The study

• Authors: P.L. Haslam, A. Lukoszek, J.A. Merchant, M. Turner-Warwick
• Journal: Clinical and Experimental Immunology
• Published: 1978;31(2):178-88
• Cited by: 51 articles, as counted by NIH iCite
• Read it: PubMed · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 001086).

Abstract

Quantitative impairment of lymphocyte responses to phytohaemagglutinin (PHA) has been demonstrated in six (21%) out of twenty-eight patients with asbestos-associated pulmonary fibrosis, in comparison with a group of unexposed normal controls. The impairment tended to occur in patients with fairly severe fibrosis, comparatively short duration of exposure to asbestos dust and with increases in serum immunoglobulin levels. One patient with asbestosis and an associated bronchial carcinoma also had depressed lymphocyte responses to PHA. These findings suggest a relationship between defective T-lymphocyte function and the fibrotic response in asbestosis. Whether it is also linked with the development of lung cancer, occurring either before or at a pre-clinical stage of tumour growth, and is of value in identifying patients especially at risk should now be explored in longitudinal studies. However, eight out of ten patients with asbestos-associated pleural mesothelioma and without lung fibrosis showed no evidence of impaired cellular immunity, either by in vitro testing with PHA or by vivo delayed hypersensitivity skin testing, indicating that impaired T-lymphocyte function is unlikely to be a common finding in all types of asbestos-associated malignancy.

In plain English

This laboratory study, from the Brompton Hospital in London, tested whether people with asbestos-related disease had weakened T-lymphocytes, a type of white blood cell involved in immunity. The authors measured how blood lymphocytes responded to a stimulating substance, phytohaemagglutinin (PHA), and compared the results with 36 healthy volunteers who had not been exposed to asbestos. Responses were impaired in six (21%) of 28 male asbestos-exposed workers with asbestosis (scarring of the lungs). The group's average response was significantly lower than the controls' average. Impairment tended to occur in workers with more severe scarring, raised antibody (immunoglobulin) levels and shorter exposure, but these trends were not statistically significant. One patient with asbestosis and bronchial carcinoma had markedly impaired responses. Ten patients with pleural mesothelioma were also tested; eight of them had a history of asbestos exposure. Two of the ten showed slight impairment, and all ten showed delayed skin reactions to common test substances. The authors concluded that the study suggests a link between impaired T-lymphocyte function and the scarring process in asbestosis. They said any link with lung cancer must remain speculative for now.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory comparison of patient groups with healthy controls, using blood lymphocyte responses to PHA (described by the authors as preliminary studies), plus skin tests in some patients
• Who was studied: 28 male asbestos-exposed workers aged 37 to 71 who had been referred to the Pneumoconiosis Medical Panel for assessment of suspected asbestosis. Of these, 13 had moderate or severe radiographic asbestosis, 13 had minimal abnormality and 2 had normal radiographs. The study also included 1 patient with asbestosis and lung cancer and 10 patients with pleural mesothelioma (8 with a history of asbestos exposure). Controls were 36 healthy medical or laboratory staff volunteers with no asbestos exposure. The work was done at the Cardiothoracic Institute, Brompton Hospital, London.
• Exposure: Occupational exposure to asbestos dust (fiber types not specified). In the 28 workers with asbestosis, exposure lasted 22 years on average (s.d. 11 years), with a range of 2 to 42 years.
• Main results:
  • Lymphocyte responses to PHA were impaired in 6 (21%) of the 28 patients with asbestos-associated pulmonary fibrosis.
  • The mean PHA response of the asbestosis group was significantly lower, at all PHA doses tested, than the mean for the 36 controls or for 16 male controls of comparable age.
  • In the asbestosis group, two patients had abnormally low blood lymphocyte counts. The group's mean count was slightly reduced, but the reduction was not statistically significant.
  • Some features tended to go with impaired PHA responses in asbestosis patients: raised serum immunoglobulins, radiographic grade 2/1 or greater, and slightly shorter exposure. None of these trends was statistically significant.
  • Impaired PHA response in asbestosis patients was not associated with ANA or rheumatoid factor antibodies, HLA 27, age or smoking.
  • The one patient with asbestos-associated lung carcinoma had markedly impaired PHA responses but still showed delayed skin responses to common antigens.
  • Among the 10 pleural mesothelioma patients, 2 (20%) had slightly impaired PHA responses, and the group's mean PHA response was significantly reduced at all doses.
  • The mesothelioma group's mean blood lymphocyte count was significantly lower than normal (p less than 0.01).
  • All 10 mesothelioma patients showed delayed hypersensitivity skin responses to common antigens.
• The authors' conclusion: The authors concluded that the study suggests a link between impaired T-lymphocyte function and the fibrotic (scarring) process in asbestosis. They added that impaired T-lymphocyte function is unlikely to be common in all types of asbestos-associated malignancy.
• Limitations the authors state:
  • The patient numbers were small; the trends linking impaired responses to disease severity, immunoglobulins and exposure duration did not reach statistical significance.
  • Any link between depressed cellular immunity and lung cancer remained speculative, and the authors called for longitudinal studies.
  • Although blood cells were washed, blocking factors that suppress the lymphocyte response might still have been present.
  • The reduced mean PHA response in the mesothelioma group was probably due to the method's sensitivity to lower lymphocyte numbers in whole blood.
  • Skin tests were not performed in the patients with asbestosis.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Pleural Mesothelioma, Pulmonary Fibrosis, Fibrosis, Carcinoma, Lung Cancer.

Related studies

• In vitro depression of human lymphocyte mitogen response (phytohaemagglutinin) by asbestos fibres — R.G. Barbers, W.W. Shih, et al. (1982)
• Response to comment on 'Existing prognostic models, but not neutrophil-to-lymphocyte ratio, are prognostic in malignant mesothelioma' — T.M. Meniawy, J. Creaney, et al. (2014)
• Sequential immunological studies in an asbestos-exposed population. II. Factors affecting lymphocyte function — M.J. Campbell, M.M. Wagner, et al. (1980)
• Aryl hydrocarbon hydroxylase induction in mitogen-stimulated lymphocytes by benzanthracene or cigarette tars adsorbed to asbestos fibers — T.L. McLemore, W.T. Jenkins, et al. (1979)
• Pulmonary and systemic immunoregulatory changes during the development of experimental asbestosis — M. Rola-Pleszczynski, S. Gouin, et al. (1984)
• High blood neutrophil-to-lymphocyte ratio is an indicator of poor prognosis in malignant mesothelioma patients undergoing systemic therapy — S.C. Kao, N. Pavlakis, et al. (2010)

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