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Chronic asthma, a worrying update

Once asthma is established, chronic inflammation in the lungs is a critical feature of the disease. Inflammation can be made worse by inhaling allergens or irritants (such as smoke, ozone, diesel particles) or from a respiratory viral infection.
Respiratory inflammation is the result of the body's immune system defending delicate tissue from harm. The cells that participate in this line of defence include eosinophiles and neutrophiles.

      Eosinophil activity is associated with allergy and allergic reaction or invasion by parasites
      Neutrophiles are associated with defending tissue from harm or infection

Traditionally asthma has been mainly associated with allergy, however, recent research on the new sophisticated anti-allergy drug Xolair, has found that not all symptoms of asthma are allergy related. From these results doctors now speculate that allergy accounts for about half of all symptoms. To emphasise this, they point out that 70% of adult 'late-onset' asthma is not allergy based. This means that patients, who are clinically tested and confirmed to be allergic to specific allergens can no longer be confident that their asthma symptoms are caused by exposure to these allergens. Something else is happening in asthma.

Many doctors believe it is the activity of invading neutrophiles. These are the cells designed to protect vulnerable lungs which are under attack, under repair or hindered by chronic inflammation. They believe the activity of these cells may actually prolong asthma symptoms. Neutrophiles, once activated by stimuli discharge enzymes that cause tissue damage resulting in increased inflammation. The most important of these enzymes is elastase. Recent research, funded by a major UK medical charity, describes how the major house dust mite allergen Der p1 downgrades a regulator specifically designed to dampens down the harm caused by elastase.

If the Charity's doctors are proven to be right, then the whole of asthma management must be reviewed. It may no longer be appropriate for patients to rely upon drugs that artificially open airways in harmful environments in order to prevent wheezing or coughing. Exposure to known risks can encourage neutrophil proliferation and the damaging non-allergy inflammatory activity that follows. (11,12,13,14)


  1. 'The importance of allergens in the development of asthma and the persistence of symptoms', Nelson H, Editorial, 'J.Allergy & Clin.Immun' 2000: Vol.105;(6b) Pt II
  2. 'Ozone, Airways and Allergic Airways Disease', Review. Krishna MT, Mudway F, Kelly FJ, Frew AJ, Holgate ST, 'Clin. Exper. Allergy', 1995;25:1150-1158
  3. 'Eosinophil epithelial cell interactions: a special relationship?', Editor,' Clin. Exp. Allergy', 2001, Vol. 31, 351-354
  4. Efficacy and safety of a recombinant anti-immunoglobulin E antibody (omalizumab) in severe allergic asthma. Holgate ST et al, 'Clin Exp Allergy', 2004: 34, page 632-638
  5. 'Anti-IgE therapy in allergic disease', Henry Milgrom, 'Current Opinion in Pediatrics', 2004, 16: 642-647 Notation;
  6. Please refer to reference 16 in this paper. 'Treatment with anti-IgE in the airway mucosa of asthmatics. It is associated with a marked reduction in airway eosinophilia, expression of Fce R1 and IL4. Interestingly, these changes are not accompanied by a measurable improvement in airway hyperresponsiveness.' Djukanovic R, Wilson SJ, Kraft M, 'Am J Respir. Crit. Care Med.', Published as June 1st 2004 as doi:10.1164/rccm,200312-1651OC
  7. 'Non-eosinophilic asthma: importance and possible mechanisms', Douwes J, Gibson P, Pekkanen J, Pearce N, Thorax, 2002, 57: 643-648
  8. National Asthma Campaign's 'Asthma News', 2003; 72, 'Managing asthma in later life', p 11
  9. Bronchial Epithelium as a Key Regulator of Airway Allergen Sensitisation and Remodelling in Asthma', 'American Journal of Respiratory and Critical Care Medicine', Vol. 162, 2000, pS113-117
  10. 'Allergen-induced bronchial inflammation in house dust mite allergic patients with or without asthma', Lopuha CE, Out TA, Jansen HM, Aalberse RC, van der Zee JS; 'Clin. Exp. Allergy'. 2002, 32, 1720-1727
  11. 'The cellular and mediator basis of asthma in relation to natural history'. Stephen T Holgate, 'The Lancet,' 1997, Vol. 350
  12. Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects. Bosson J et al, 'Clin. Exp.Allergy', 2003, 33:777-782
  13. British Lung Foundations' publication, Final Research Report, Grant Holder: Professor R Stockley, Researchers: Dr H Lin, ' To understand ho a damaging protein called neutrophil elastase, which is released by white blood cells as part of the lungs' protective response system in made.' Sponsored by Allen & Hamburys
  14. 'House Dust Mite Der p 1 Downgrades Defenses of the Lung by Inactivating Elastase Inhibitors', Brown A, et al, 'Am.J.Respir.Cell Mol. Biol',. 2003, 29; 381-389
  15. 'Elafin (elastase-specific inhibitor) has anti-microbial activity against Gram-positive and Gram-negative respiratory pathogens\', Simpson AJ, Maxwell AI, Govan JRW, Haslett C, Sallenave JM,; 'FEBS Letters', 452 (1999) 309-313