International Journal of Inflammation, Cancer and Integrative Therapy
Open Access

Atopic dermatitis (AD), also known as eczema, is a chronic inflammatory skin condition characterized by itchy, dry, and scaly skin. Its prevalence has been increasing globally, affecting both children and adults. The etiology of AD is complex, involving genetic, environmental, and immunological factors. Recent research has highlighted the potential role of the skin microbiome in the pathogenesis of AD. The skin microbiome, which consists of a diverse community of bacteria, fungi, viruses, and other microorganisms, plays a crucial role in maintaining skin health and influencing immune responses. Dysbiosis, or an imbalance in the microbial communities, has been implicated in various skin disorders, including AD. This review aims to explore the relationship between bacterial flora and atopic dermatitis, emphasizing the mechanisms through which microbial imbalances may contribute to the development and exacerbation of the condition [1].

Description

The skin microbiome and its role

The skin microbiome is a dynamic ecosystem with a diverse range of microorganisms that include bacteria, fungi, and viruses. Bacteria are the most studied components of the skin microbiome. Common skin bacteria include Staphylococcus epidermidis, Staphylococcus aureus, Propionibacterium acnes, and Corynebacterium species. These microorganisms contribute to the skin’s barrier function, modulate local immune responses, and compete with pathogenic organisms.

In healthy skin, there is a balanced and stable microbiome that supports skin homeostasis and immune function. However, disruptions in this balance, such as an overgrowth of pathogenic bacteria or a reduction in beneficial species, can lead to skin diseases.

Bacterial flora in atopic dermatitis

Research has demonstrated significant alterations in the skin microbiome of individuals with AD. Notably, an increase in the abundance of Staphylococcus aureus has been consistently observed in AD patients. S. aureus is known for its ability to produce toxins that can exacerbate inflammation and disrupt skin barrier function. The overgrowth of S. aureus in AD skin may be associated with increased susceptibility to secondary infections and further aggravation of dermatitis [2].

Conversely, a reduction in the diversity of beneficial skin bacteria, such as S. epidermidis and Corynebacterium species, has been reported in AD patients. These beneficial bacteria are thought to play a role in maintaining skin integrity and modulating immune responses. The loss of these protective microbes can lead to an imbalance that promotes inflammation and disease progression.

Mechanisms linking bacterial flora and atopic dermatitis

Several mechanisms have been proposed to explain how bacterial dysbiosis contributes to AD. These includes

Immune modulation: Bacteria influence the local immune environment of the skin. Pathogenic bacteria like S. aureus can trigger inflammatory responses by activating innate immune cells and releasing pro-inflammatory cytokines. In contrast, beneficial bacteria help regulate immune responses and maintain tolerance [3].

Barrier function disruption: The skin barrier is crucial for protecting against environmental insults and preventing pathogen entry. Disruptions in the skin microbiome can impair barrier function, making the skin more susceptible to irritants and allergens. For example, S. aureus produces enzymes that degrade skin lipids, weakening the barrier [4].

Toxin production: S. aureus and other pathogens can produce toxins that exacerbate inflammation and damage skin tissues. These toxins can further impair the skin barrier and contribute to the chronicity of AD.

Therapeutic implications

Understanding the link between bacterial flora and AD has led to the exploration of microbiome-based therapies. Probiotics, prebiotics, and topical antimicrobial agents are being investigated for their potential to restore microbial balance and alleviate AD symptoms [5]. For example, probiotic treatments aimed at increasing beneficial bacteria or reducing pathogenic strains may offer new therapeutic options for managing AD. Additionally, interventions that focus on improving skin barrier function and reducing inflammation may help in managing the condition more effectively [6].

Conclusion

The relationship between bacterial flora and atopic dermatitis is an area of active research with significant implications for understanding and treating this common skin condition. Dysbiosis of the skin microbiome, characterized by an overgrowth of pathogenic bacteria and a reduction in beneficial species, appears to play a crucial role in the pathogenesis and exacerbation of AD. The mechanisms through which bacterial imbalances influence AD involve immune modulation, disruption of skin barrier function, and toxin production.

As research continues to elucidate these mechanisms, it is hoped that microbiome-based therapies will emerge as effective treatments for AD. Restoring microbial balance and enhancing skin barrier function could offer promising avenues for managing this challenging condition. Further studies are needed to better understand the complex interactions between skin bacteria and the host immune system, and to develop targeted interventions that can improve the quality of life for individuals suffering from atopic dermatitis.

Acknowledgement

None

Conflict of Interest

None

References

1. Ni L, Dong C (2017) New checkpoints in cancer immunotherapy. Immunol rev 276: 52-65.

Indexed at, Google Scholar, Crossref

2. Li X, Hu W, Zheng X, Zhang C, Du P, et al. (2015) Emerging immune checkpoints for cancer therapy. Acta Oncologica 54: 1706-1713.

Indexed at, Google Scholar, Crossref

3. Topalian SL (2017) Targeting immune checkpoints in cancer therapy. Jama 318: 1647-1648.

Indexed at, Google Scholar, Crossref

4. Lee L, Gupta M, Sahasranaman S (2016) Immune Checkpoint inhibitors: An introduction to the next‐generation cancer immunotherapy. J Clin Pharmacol 56: 157-169.

Indexed at, Google Scholar, Crossref

5. Sadreddini S, Baradaran B, Aghebati‐Maleki A, Sadreddini S, Shanehbandi D, et al. (2019) Immune checkpoint blockade opens a new way to cancer immunotherapy. J cell physiol 234: 8541-8549.

Indexed at, Google Scholar, Crossref

6. Swatler J, Kozłowska E (2016) Immune checkpoint‑targeted cancer immunotherapies. Postepy Hig Med Dosw 70: 25-42.

Indexed at, Google Scholar, Crossref