[1] These microbial infections result in chronic lower airway inflammation, impaired mucociliary clearance, an increase in mucous production and eventually asthma.
Furthermore, children who experience severe viral respiratory infections early in life have a high possibility of having asthma later in their childhood.
[2] As a result, inflammation and associated healing process leads to scar formation and tissue remodelling, which are symptoms that can be found in almost all asthmatics patients.
[3][4] A recent meta-analysis reported that the overall population attributable risk for C. pneumoniae-specific IgE in chronic asthma was 47% and was strongly and positively associated with disease severity.
[9] C. pneumoniae infection may not only be persistent and chronic, but it also has irreversible tissue injury and scarring processes,[2] which are symptoms in asthma patients.
[2] Meanwhile, sero-epidemiological data also provide evidences to support that C. pneumoniae plays a role in asthma by amplifying inflammation and inciting the disease process.
[2] Its antigenic stimulation strongly amplifies chronic inflammation by increasing the production of proinflammatory cytokines, tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IFN-γ by infected cells, which ultimately leads to immunopathological tissue damage and scarring in the asthmatic lungs.
[7] Most strikingly, a recent systematic review and meta-analysis found that C. pneumoniae-specific IgE was associated with almost half of the asthma cases studied.
[10] Mycoplasma pneumoniae is a bacterium that belongs to the phylum Firmicutes, class Mollicutes, order Mycoplasmatales and family Mycoplasmataceae.
It is an extracellular, host-associated bacterium that lacks a cell wall[12] and is unable to survive outside of a host due to osmotic instability in the environment.
It is a parasitic bacterium that invades the mucosal membranes of the upper and lower respiratory tract, including nasopharynx, throat, trachea, bronchi, bronchioles, and alveoli.
The injury of host epithelial cells caused by M. pneumoniae adhesion is thought to be due to the production of highly reactive species: hydrogen peroxide (H2O2) and superoxide radicals (O2–).
The intracellular existence of M. pneumoniae could facilitate the establishment of latent or chronic states, circumvent mycoplasmacidal immune mechanisms, its ability to cross mucosal barriers and gain access to internal tissues.
Besides, Nisar et al. (2007) also adds that M. pneumoniae infection causes pulmonary structural abnormalities, resulting in a decrease in expiratory flow rates and an increase in airways hyper-responsiveness in non-asthmatic individuals.
The release of proinflammatory cytokines in response to M. pneumoniae infection has been indicated as a possible mechanism leading to bronchial asthma.
[12] This is because the increase of cytokine production results in a continuing inflammatory response in the airway, followed by negative effects such as immunopathological tissue damage and scarring as described in the C. pneumoniae's role in asthma section.
Similarly, M. pneumoniae infection promotes a T helper type 2 response, which is why M. pneumoniae-positive patients with asthma have increased airways expression of tumour necrosis factor a, IL4 and IL5.
The T helper type 2 predominant airways disease caused by M. pneumoniae infection may lead to IgE-related hyper-responsiveness and eosinophil function, resulting in an onset of asthma.
[13] A study done by Laitinen et al. (1976) suggests that M. pneumoniae infection denude the epithelial surface and expose irritant receptors.
[15] Asthmatic subjects in 9 to 11 years old, 80% to 85% of asthma exacerbations that were associated with reduced peak expiratory flow rates and wheezing were due to viral upper respiratory tract infections (URIs).