Indian Journal of Dermatology
: 2021  |  Volume : 66  |  Issue : 4  |  Page : 438--440

Inflammasome Related Mediators and Their Association with Disease Determinants in Chronic Plaque Psoriasis

Seema Chhabra1, Tarun Narang2, Frainey Bansal1, Smrity Sahu1, Sunil Dogra2,  
1 Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Sunil Dogra
Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh

How to cite this article:
Chhabra S, Narang T, Bansal F, Sahu S, Dogra S. Inflammasome Related Mediators and Their Association with Disease Determinants in Chronic Plaque Psoriasis.Indian J Dermatol 2021;66:438-440

How to cite this URL:
Chhabra S, Narang T, Bansal F, Sahu S, Dogra S. Inflammasome Related Mediators and Their Association with Disease Determinants in Chronic Plaque Psoriasis. Indian J Dermatol [serial online] 2021 [cited 2022 May 22 ];66:438-440
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Full Text


Psoriasis vulgaris (PV) is characterized by immune dysregulation leading to inappropriate activation of proinflammatory cytokines. In plaque-type psoriatic lesions, keratinocytes express IL-1β and IL-18 which regulate the expression of genes involved in the pathogenesis of psoriasis.[1] The biologic activity of these cytokines is regulated by inflammasomes through caspase 1 activation.[2] Inflammasomes are large intracellular multi-protein signaling complexes which are formed in response to diverse pathogenic stimuli and constitute a central nucleus around which the inflammatory response develops. These multimeric complexes consist of an assembly of three elements: a sensor protein (receptor), an adaptor protein, and an effector protein (caspases). This assembly generates an inflammatory response resulting in the production of IL-18 and IL-1β.[2] Normal inflammasome response is needed for an effective innate immune response but its exaggerated activity leads to deleterious effects on the organism resulting in a variety of immune-mediated and autoimmune conditions including psoriasis.[3] The present study was undertaken in PV patients to attempt to delineate the pattern of circulating markers of inflammasome activity (IL-1β, IL-18) and their relationship with disease determinants.

This prospective case-control study was performed on 40 newly registered consenting PV patients and 17 age- and sex-matched (P = 0.457 and 0.464, respectively) healthy controls. Demographic and disease data were recorded. Psoriasis area severity index (PASI) scores were determined at the initial visit. All included patients were outside a washout period of 2 months from systemic and 2 weeks from topical medication. Patients with known autoimmune disease, malignancy, or serious chronic systemic disease and pregnant and lactating women were excluded. The study was approved by the institutional ethics committee PGIMER, Chandigarh (PGI/IEC/2015/1507 dated 15-10-2015).

Whole blood samples (3 mL) were collected in plain tubes and sera were separated and stored at −80°C. Enzyme linked immunosorbent assay (ELISAs) for IL-18 (RayBiotech, GA, USA) and IL-1β (E biosciences, California, USA) were performed per manufacturer guidelines. Patients were stratified by sex (males vs. females), age at onset (early [≤40years] vs. late [>40 years]), severity (mild-to-moderate vs. severe; depending on the PASI scores), disease duration (≤5 vs. >5 years), associated systemic comorbidities, and disease status (stable vs. unstable). All statistical tests were performed using the IBM SPSS (version 22.0) software at a significance level of α =0.05 after testing the normality of the variables. An analysis of correlations of the subpopulations with various disease parameters in the patients was conducted. Group comparisons were made with the Chi-square test or Fisher's exact test.

[Table 1] summarizes the clinical characteristics of the patients. Most patients (n = 33, 82.5%) had early-onset disease. Patients with longer disease duration showed more severe disease (P = 0.032). Serum levels of IL-1β and IL-18 were significantly higher in patients (0.41 ± 0.38 and 34.4 ± 12.2 pg/mL, respectively) compared to controls (0.19±0.20 and 23.6 ± 7.9, respectively) (P < 0.05*) [Figure 1]. Individual cytokine levels were compared in different patient subgroups [Figure 2]. Neither cytokine showed a statistically significant correlation with disease severity. Serum IL-18 levels were found to be higher in patients with late-onset psoriasis (P = 0.044*). Patients with comorbidities showed statistically significant higher levels of both cytokines (P < 0.05). No significant correlations were observed between the cytokine concentrations and sex, duration, or disease status (P > 0.05).{Figure 1}{Figure 2}{Table 1}

Pietrzak et al.[4] observed significantly increased plasma IL-18 concentrations showing a linear correlation with PASI scores. They reported more severe disease (PASI scores 15–48) in their cohort of 12 patients.[4] We also found significantly increased levels of these cytokines in our group of North Indian psoriatic patients (n = 40) indicating their systemic activation. However, we did not observe any correlation with disease severity: most patients (n = 35) in our cohort had mild-to-moderate disease (mean PASI scores 4.02 ± 2.7), with only five patients having PASI>10.

Varma et al.[5] have also not observed any correlations between plasma levels of inflammasome-generated IL-1β and IL-18 with PASI scores in their cohort suggesting that the cutaneous manifestations are independent of inflammasome-dependent systemic inflammation.

The complex nature of PV worsens the patient's quality-of-life due to its association with other comorbidities and vascular complications.[6] In this study, serum cytokine levels were significantly elevated in patients with associated comorbidities as compared to those without, reiterating the fact that a systemic inflammatory state, with proinflammatory cytokines as potential coadjuvants, is a possible link between psoriasis and systemic comorbidities.[7]

Increased systemic levels of these proinflammatory cytokines exacerbate the systemic inflammatory process—a hallmark of PV.[6] Inflammasomes have been recently documented as important players in triggering systemic inflammation in psoriasis.[5] Moreover, IL-18 may be involved in the formation of Munro microabscesses and plaques.[8] Studies linking inflammasome activation and consequently increased proinflammatory cytokine production with Th17 responses might shed light onto newer molecular mechanisms of psoriasis pathogenesis, and help establish newer therapeutic and preventive approaches, ultimately improving the outcome for psoriatic patients.


Special thanks to Dr. Neha Joshi for her valuable suggestions regarding the study.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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