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Immunomodulatory Tissue Factors in the Gallbladder Walls of Pediatric Patients with Chronic Calculous Cholecystitis
Kaiva Zīle Zariņa1, Māra Pilmane1, Aigars Pētersons2
1Institute of Anatomy and Anthropology, Riga Stradins University, Kronvalda Boulevard 9, LV-1010 Riga, Latvia.
Insights
Pediatric chronic calculous cholecystitis involves key immune factors like NFkBp65, IL-12, and HSP60. Sonic hedgehog protein (SHH) also plays a role in tissue repair and inflammation in these cases.
Area of Science:
- Immunology
- Gastroenterology
- Pediatric Surgery
Background:
- Rising rates of gallstones and cholecystectomy in children highlight concerns about chronic cholecystitis.
- The exact mechanisms behind pediatric calculous cholecystitis are not fully understood.
Purpose of the Study:
- To investigate the expression and distribution of specific immunomodulatory factors in pediatric chronic calculous cholecystitis.
- Key factors studied include IL-12, IL-13, IL-1β, SHH, NFkBp65, and HSP60.
Main Methods:
- Immunohistochemistry was used to detect target factors in gallbladder tissue.
- Samples from 11 pediatric patients and 5 healthy controls were analyzed.
- Semi-quantitative assessment and statistical analysis (Mann-Whitney U, Spearman correlation) were performed.
Main Results:
- Significant differences in IL-1β, SHH, and NFkBp65 expression were found in the epithelium between patients and controls.
- Elevated expression of IL-12, SHH, and HSP60 was observed in the vasculature of patient samples.
- IL-1β expression was higher in controls, while other markers were more prominent in patients.
Conclusions:
- Increased NFkBp65, IL-12, and HSP60 suggest a role in immune modulation and sustained inflammation in pediatric calculous cholecystitis.
- SHH expression indicates involvement in tissue repair, inflammation, and vascular responses.
- Coordinated interactions among these factors are crucial for the disease's development.
Background:
The rising rates of gallstones and cholecystectomy in pediatric populations underscore the increasing concern regarding chronic cholecystitis. However, the morphopathogenesis of pediatric calculous cholecystitis is still not well understood. This study aimed to determine the expression and distribution of immunomodulatory factors interleukin-12 (IL-12), interleukin-13 (IL-13), interleukin-1β (IL-1β), sonic hedgehog protein (SHH), nuclear factor NF-kappa-B p65 subunit (NFkBp65), and heat shock protein 60 (HSP60) in the gallbladder walls of pediatric patients with chronic calculous cholecystitis.
Methods:
In total, 11 gallbladder samples were collected from pediatric patients with calculous cholecystitis during cholecystectomy, while 5 healthy gallbladder samples served as controls. IL-12, IL-13, IL-1β, SHH, NFkBp65, and HSP60 were detected by immunohistochemistry. The number of positive structures in gallbladder wall epithelium, vasculature, and inflammatory infiltrate was assessed semi-quantitatively by microscopy. A Mann-Whitney U test and Spearman's rank-order correlation coefficient were calculated.
Results:
Statistically significant differences were observed between patient and control samples in the expression of IL-1β, SHH, and NFkBp65 in the epithelium, as well as in the expression of IL-12, SHH, and HSP60 in the blood vessels. The expression of IL-1β was stronger in the epithelium of controls, while other markers were more prominent in patient samples.
Conclusions:
An increased number of NFkBp65, IL-12, and HSP60 positive cells in patient gallbladder tissue suggests a significant role of these tissue factors in driving immune modulation and sustaining the inflammation in pediatric chronic calculous cholecystitis. The noticeable expression of SHH in patient gallbladder tissue indicates its part in tissue regeneration and repair processes, as well as in modulating inflammation and vascular responses in calculous cholecystitis. The significant positive correlations between the factors studied highlight the importance of their coordinated interaction and intricate crosstalk in the morphopathogenesis of calculous cholecystitis.
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