ISSN ONLINE(2319-8753)PRINT(2347-6710)

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

A Microbiological Study on Asthma and Allergy Management

1Rajesh Kr Dubey2Preeti Katiyar, 3Akash Dipanker, 4Ricky Ritesh Tuck, 5Sunita Arya
  1. Director, PERI, Lucknow-226012,UP, India
  2. Research Scholar, ShriVenkateshwara University, Gajraula, UP, India.
  3. M.P.N. Degree College, OsiyanUnnao, UP, India
  4. Research Scholar, ShriVenkateshwara University, Gajraula, UP, India
  5. Assistant Professor, DGPG College, Kanpur, UP, India
Related article at Pubmed, Scholar Google

Visit for more related articles at International Journal of Innovative Research in Science, Engineering and Technology


The compare of allergic disorders between populations in different countries by sing standard validated questions, thereby providing a framework for research into possible modifiable lifestyle and environmental factors affecting these disorders that may ultimately lead to a reduction in the personal burden of allergic diseases. Many centres from developing countries were able to participate in the simplicity. The data provides a unique illustration of the prevalence of current symptoms of asthma, rhino conjunctivitis and eczema in children and adolescents worldwide


Antimicrobial peptides;Immunomodulatory;Lymphopoietin;Antibiotics.


There is a wide consensus that the prevalence of asthma and allergies are on the increase among children worldwide. In some industrialized countries, asthma and allergies have reached alarming proportions, affecting up to one-third of children within the general population. In addition, few of the studies of prevalence were completed in developing countries. A Study of Asthma and Allergies has developed a standardized methodology to describe the prevalence and severity of symptoms of asthma, rhino conjunctivitis and eczema in the world.In the development of both asthma and allergic rhinoconjunctivitis, there is a complex interaction of genetic and environmental factors. A possible explanation is the “hygiene hypothesis”. This suggests that increased hygiene and the resulting lack of exposure to various microorganisms in early life affect the immune system so that individuals’ ability to fight off certain diseases is weakened and they are more susceptible to autoimmune diseases.
Good management of asthma can control the disorder and enable people to enjoy a high quality of life. Early diagnosis and appropriate treatment lead to much better disease control and outcomes. Allergy can be progressive, and neglecting its symptoms may lead to a worsening of the disease. Medication is not the only way to control asthma and allergies. It is also important to avoid triggers that irritate and inflame the airways. Primary prevention to reduce the level of exposure to common risk factors, particularly tobacco smoke, frequent lower respiratory infections during childhood and air pollution (indoor and outdoor), is an important step.


The identification of key microorganisms that are linked with asthma development or asthma pathogenesis raises the important question of which properties of these microorganisms promote asthma. Some of these microorganisms may be found systemically in more severe disease, as has been shown for RVs73. A key feature of a microorganism in promoting asthma is the ability to induce lung inflammation, injury, or repair and remodeling. Many of the innate receptors that recognize respiratory fungi, viruses or bacteria, including TLRs, RIG-I-like helicases and NOD-like receptors activate the nuclear factor-κB (NF-κB) family of transcription factors, which induce more than 100 pro-inflammatory and host response genes74. RSV and RVs induce a range of pro-inflammatory cytokines, chemokine’s, growth factors, adhesion molecules and mucins. Mucins cause mucous plugging of the airway and may provide a substrate for bacterial colonization, whereas cytokines facilitate cellular chemo taxis, and activation and proliferation of immune cells in the infected airway45, 75. Microorganisms may damage and compromise the integrity of the airway by infecting airway epithelial cells, causing cell death76 and shedding77. They can also affect epithelial permeability, leading to increased airway inflammation and creating opportunities for increased infection78, allergen uptake79 or exposure to environmental pollutants, all of which are important contributing factors in asthma.
Microorganisms and asthma treatment
Asthma treatment often requires daily treatment with a range of immunomodulatory or immunosuppressive agents, such as macrolide antibiotics or glucocorticoids, suggesting another way that microorganisms interact with asthma. Surprisingly, scant attention has been paid to the possible effects of such treatments on an individual’s micro biota and their antimicrobial responses. However, some studies provide indirect evidence for an immunosuppressive effect. For example, increases in bacterial pneumonia have been noted in patients with COPD who are treated with glucocorticoid therapy84. Furthermore, an increased incidence of upper respiratory tract infections following treatment with the leukotriene receptor antagonist montelukast has been reported in young children with asthma85. It is also interesting to speculate whether the fact that asthma is a risk factor for IPI, as previously discussed, is directly attributable to asthma therapies such as glucocorticoids. Conversely, there is some experimental evidence suggesting that the action of glucocorticoids confers benefits to antimicrobial immunity. In vitro, glucocorticoids have been shown to induce a number of antimicrobial peptides, pentraxins, and collections and complement proteins.


An increasing trend in the prevalence of asthma and allergies is particularly apparent in urban areas, where children have been found to have more allergic reactions to outdoor and indoor allergens.
Asthma phenotype Description
Atopic (allergic) asthma • Reactivity to one or more known allergens (determined by skin prick test)
• Higher than normal IgE levels
• Specific IgE to allergen (determined by radioallergosorbent assay*)
• Eosinophils in the airways (common but not always)
Non-allergic asthma • No known allergy
• No or low serum IgE
• No reactivity to allergen (determined by skin prick test or radioallergosorbent assay*)
Mild asthma • Occasional symptoms, but well controlled by therapy (low-dose glucocorticoids and/or short-acting β2 agonists)
Stable asthma • Well-controlled symptoms
• No dysregulated lung function or asthma exacerbations
Severe asthma • Poor control of symptoms despite using maximal therapy (high-dose glucocorticoids and/or β2 agonists, or other therapies)
Asthma exacerbations • Mild or severe asthma with sudden symptom onset, often requiring medical consultation or hospitalization and possible oral glucocorticoid intervention
Neutrophilic asthma • Increased number of neutrophils in bronchoalveolar lavage or sputum samples (can be allergic or non-allergic asthma)
Allergic bronchopulmonaryaspergillosis • Invasive colonization of the airway with Aspergillusspp., an opportunistic pathogen;
Virus-induced wheeze or bronchiolitis • Common in young children (<2 years of age)
• Asthma caused by a viral infection, mucus and inflammation in young children, giving a typical ‘wheezy’ episode
• Mild, severe, acute onset or febrile
High TH2-associated atopic asthma • TH2 cell-associated gene expression is typical (for example, expresses IL13 and IL-13-inducible genes)
• Responds well to glucocorticoids
• Prone to asthma exacerbations135
Low TH2-associated atopic asthma • A mixed phenotype of asthma
• Less prominent TH2 type cytokine responses
• More refractory to glucocorticoid treatment than patients with high TH2-associated atopic asthma135
There seems to be a parallel development between climate change and the increasing prevalence of asthma and allergies in children. As warmer temperatures and early spring are related to increased airborne pollen, sensitization to pollen allergens is likely to have doubled during the last three decades, particularly in young people in many areas.


Microbiological involved in asthma and their niches
A cross-section of the human lower respiratory tract, showing sites of infection for different microbiological effects that they have on airway function. This would also be facilitated by an increase in tertiary lymphoid tissue in the lung parenchyma, which is a common feature following respiratory tract infection104, in human asthma105 and in experimental mouse models of asthma106.
Successive infections may also alter the lung environment and affect the delicate balance between host, pathogen and chronic airway disease. Bacterial infections are known to follow influenza virus infections; indeed, many of the individuals who died in the influenza pandemics exhibited coexisting bacterial pneumonia107. This has implications for asthma: what is assumed to be a virus-induced asthma exacerbation may in fact include a secondary bacterial infection. Data suggesting that this does occur have been reported for C. pneumoniae69, but further studies are required to determine whether secondary bacterial infections commonly follow viral infections in asthma. Thus, by causing barrier disruption, viruses may initiate a cascade that, as described above, allows environmental bacteria better access to the underlying tissue.
Respiratory viruses interact with allergens in an additive or synergistic manner, promoting asthma
Following sensitization, allergen presentation by airway dendritic cells (DCs) facilitates the promotion of T helper 2 (TH2) cells. Viruses infect epithelial cells, stimulating the release of TH2 cell-promoting chemokines CC-chemokine ligand 17 (CCL17) and CCL22, and cytokines thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25) and IL-33. The TH2 type chemokines attract TH2 cells into the airway, and these in turn secrete IL-4, IL-5 and IL-13. IL-5 promotes eosinophilia, and the resultant eosinophils release the inflammatory mediator’s major basic protein (MBP), eosinophil cationic protein (ECP) and transforming growth factor-β (TGFβ), inducing inflammation in the airway smooth muscle (ASM). IL-4 and IL-13 cause antibody class switching to immunoglobulin E in B cells, so that B cells secrete allergenspecific IgE. This antibody then binds mast cells, and crosslinking of the allergen on mast cell-bound IgE causes mast cell degranulation and release of preformed mediators, including histamine, prostaglandin (PGD2) and leukotrienes (LTC4, LTD4 and LTE4). These mediators cause bronchoconstriction and further airway inflammation. Mast cells also produce the TH2 cytokines IL-4 and IL-13, as well as other cytokines, including TGFβ and tumour necrosis factor (TNF), promoting further TH2 type immune responses and inflammation.


Although several studies support the use of macrolide antibiotics for the treatment of atypical pathogens in patients with asthma exacerbations88, it is important to consider how the microbiological is affected by macrolides or other antibiotics and how this might affect asthma and the host responses to infection. Treatment of mice with the antibiotics vancomycin, neomycin, metronidazole and ampicillin greatly changes their airway and gut microbiological and impairs their antiviral responses to influenza viruses35. In human studies, it is currently unclear whether the genera that seems to colonize the airways of patients with asthma or and of individuals without asthma or differ because of treatment-specific effects34. More research is needed to understand whether the microbiological of patients with asthma is actually a consequence of active therapy. Further large clinical trials with such treatments are required to understand the relationships between microbiological and asthma treatments.


The empirically driven realization that allergy and asthma are intertwined demand a greater understanding of the cellular components of these and of the mechanisms that regulate them. Whether adenosine is the key component that links allergy and asthma remains to be determined.


1. Lambrecht BN, Kool M, Willart M, Hammad H: Mechanism of action of clinically approved adjuvants. Curr. Opin. Immunol. 2009, 21:23–9. Pulendran B, Tang H, Manicassamy S: Programming dendritic cells to induce T(H)2 and tolerogenic responses. Nat. Immunol. 2010, 11:647– 55.

2. Ohtani T, Nakagawa S, Kurosawa M, Mizuashi M, Ozawa M, Aiba S: Cellular basis of the role of diesel exhaust particles in inducing Th2- dominant response. J. Immunol. 2005, 174:2412–9.

3. Todd DJ, Lee A, Glimcher LH: The endoplasmic reticulum stress response in immunity and autoimmunity. Nat. Rev. Immunol. 2008, 8:663– 74.

4. Banchereau J, Steinman RM: Dendritic cells and the control of immunity. Nature. 1998, 392:245–52.

5. Hammad H, Plantinga M, Deswarte K, Pouliot P, Willart M, Kool M, Muskens F, Lambrecht BN: Inflammatory dendritic cells--not basophils-- are necessary and sufficient for induction of Th2 immunity to inhaled house dust mite allergen. J. Exp. Med. 2010, 207:2097–111.

6. Lambrecht BN, Salomon B, Klatzmann D, Pauwels RA: Dendritic cells are required for the development of chronic eosinophilic airway inflammation in response to inhaled antigen in sensitized mice. J. Immunol. 1998, 160:4090–7.

7. vanRijt LS, Jung S, Kleinjan A, Vos N, Willart M, Duez C, Hoogsteden HC, Lambrecht BN: In vivo depletion of lung CD11c+ dendritic cells during allergen challenge abrogates the characteristic features of asthma. J. Exp. Med. 2005, 201:981–91.

8. vanRijt LS, Vos N, Willart M, Muskens F, Tak PP, van der Horst C, Hoogsteden HC, Lambrecht BN: Persistent activation of dendritic cells after resolution of allergic airway inflammation breaks tolerance to inhaled allergens in mice. Am. J. Respir. Crit. Care Med. 2011, 184:303– 11.

9. Smith KA, Hochweller K, Hämmerling GJ, Boon L, MacDonald AS, Maizels RM: Chronic helminth infection promotes immune regulation in vivo through dominance of CD11cloCD103- dendritic cells. J. Immunol. 2011, 186:7098–109.

10. Kool M, Soullié T, van Nimwegen M, Willart M, Muskens F, Jung S, Hoogsteden HC, Hammad H, Lambrecht BN: Alum adjuvant boosts adaptive immunity by inducing uric acid and activating inflammatory dendritic cells. J. Exp. Med. 2008, 205:869–82.

11. Kool M, Willart M, van Nimwegen M, Bergen I, Pouliot P, Virchow JC, Rogers N, Osorio F, Reis E, Sousa C, Hammad H, Lambrecht BN: An unexpected role for uric acid as an inducer of T helper 2 cell immunity to inhaled antigens and inflammatory mediator of allergic asthma. Immunity. 2011, 34:527–40.

12. Jung S, Unutmaz D, Wong P, Sano G, de los Santos K, Sparwasser T, Wu S, Vuthoori S, Ko K, Zavala F, Pamer EG, Littman DR, Lang RA: In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens. Immunity. 2002, 17:211–20.

13. Lambrecht BN, de Veerman M, Coyle AJ, Gutierrez-Ramos JC, Thielemans K, Pauwels RA: Myeloid dendritic cells induce Th2 responses to inhaled antigen, leading to eosinophilic airway inflammation. J. Clin. Invest. 2000, 106:551–9.

14. Perrigoue JG, Saenz SA, Siracusa MC, Allenspach EJ, Taylor BC, Giacomin PR, Nair MG, Du Y, Zaph C, van Rooijen N, Comeau MR, Pearce EJ, Laufer TM, Artis D: MHC class II-dependent basophil-CD4+ T cell interactions promote T(H)2 cytokine-dependent immunity. Nat. Immunol. 2009, 10:697–705.

15. Sokol CL, Chu N, Yu S, Nish SA, Laufer TM, Medzhitov R: Basophils function as antigen-presenting cells for an allergen-induced T helper type 2 response. Nat. Immunol. 2009, 10:713–20.