ISSN: 2576-3881

Journal of Cytokine Biology
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  • Letter To Editor   
  • J Cytokine Biol, Vol 7(2)

Cytokines as a Clinical Therapy for Tendon Injury

Alix K Berglund*
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA
*Corresponding Author: Alix K Berglund, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA, Email: akberglund@ncsu.edu

Received: 17-Mar-2022 / Manuscript No. jcb-22-57597 / Editor assigned: 19-Mar-2022 / Reviewed: 24-Mar-2022 / QC No. jcb-22-57597 / Revised: 29-Mar-2022 / Published Date: 04-Apr-2022

Letter to Editor

In a variety of current therapies, cytokine modulation has been routinely employed to boost inherent healing processes. While other anatomical sites offer a more conclusive analysis of cytokine data, the tendon poses unique detection issues, making a thorough depiction of cytokine participation following injury impossible so far. Without this understanding, the evolution of tendon healing techniques is constrained. In this study, we cover what is known about the cytokine profile in the damaged tendon environment as well as the particular barriers to cytokine detection in the tendon, as well as potential solutions to these issuesIL-1, TNF-, and IL-6 have been identified as essential cytokines for starting tendon repair, although their function and temporal expression remain unknown. Methods for cytokine assessment in the tendon, such as cell culture, tissue biopsy, and micro dialysis, have advantages and disadvantages, but new methods and approaches are required to further this study. We conclude that future study designs for cytokine detection in damaged tendons should fulfil certain criteria in order to obtain conclusive characterisation of cytokine expression and guide future therapies [1].

Tendon injury is a common musculoskeletal condition that affects roughly 32 million people in the United States every year. Tendon injuries are common in athletic animals such as agility dogs and performance horses. Whether the damage is as severe as a full rupture or an on-going chronic tendinopathy, tendons are inherently sluggish to mend and seldom repair themselves to a totally healthy condition, causing athletes to return to training and competition substantially later. Inadequate repair of injured tissue might result in a re-injury rate of the afflicted tendon of 23–67%. The absence of a thorough knowledge of the tendinous milieu following injury in terms of the timing and presence of cytokines crucial to the healing process has hampered progress. Cytokine detection studies have been done in an attempt to answer unanswered questions; however research design problems prohibit uniform findings from being reached. Future research must strive to overcome these limitations by applying in vivo temporal cytokine detection methods in species, anatomic, and disease specific models to develop regenerative medicine for tendon damage.

The absence of a thorough knowledge of the tendinous milieu following injury in terms of the timing and presence of cytokines crucial to the healing process has hampered progress. Cytokine detection studies have been done in an attempt to answer unanswered questions; however research design problems prohibit uniform findings from being reached. Future research must strive to overcome these limitations by applying in vivo temporal cytokine detection methods in species, anatomic, and disease specific models to develop regenerative medicine for tendon damage.

Given the early introduction of TNF-, it is possible that this action on tenocytes functions as a physical modification to inhibit LXA-4 overexpression until the environment is cleaned of injured tissue. There might be a link between TNF-regression and the growth of FPR2/ALX receptors in tenocytes. Cytokines can function as indicators of cellular engagement in addition to signalling cellular injury, maintenance, or repair. Researchers can measure the state of the tendon by evaluating the concentration and specificity of these signals in their presence or absence. Currently, research are being undertaken to capture cytokine cross-talk in an attempt to determine standard levels for what makes a “normal” or healthy tendon, and which cytokines suggest this. The optimal study plan for cytokine detection for therapy development involves species-specific test animals, targeted tendons, and the diseased condition desired for therapeutic benefit. If feasible, in vivo cytokine collection should be undertaken, keeping in mind the consequences of insertional trauma on the study’s results. Finally, ideal research would study the whole cytokine environment in each phase of tendon injury inflammatory, proliferative, and remodelling, in order to provide a thorough evaluation of the inflammatory cascade. Adhering to these standards allows the gathering of data that precisely represents cytokine activity inside the wounded tendinous environment, ensuring the utmost efficiency of therapeutic development in this field of study [3-5].

References

  1. Lee N, Hui D (2003) A major outbreak of severe acute respiratory syndrome in Hong Kong . New Engl J Med 348: 1986-1994.
  2.        Indexed at, Google Scholar, Crossref

  3. Ho JC, Ooi GC, Mok TY (2003) High-dose pulse versus nonplus corticosteroid regimens in severe acute respiratory syndrome. Am J Respir Crit Care Med, 168: 1449-1456.
  4.                Indexed at, Google Scholar    Crossref

  5. Anand K, Ziebuhr J, Wadhwani P (2003) Coronavirus main proteinase (3CLpro) structure: basis for design of anti-SARS drugs. Science 300: 1763-1767.
  6.                Indexed at, Google Scholar, Crossref

  7. Sung JJ, Wu A, Joynt GM (2004) severe acute respiratory syndrome: report of treatment and outcome after a major outbreak.  Thorax 59: 414-420.
  8.               Indexed at, Google Scholar, Crossref

Citation: Berglund AK (2022) Cytokines as a Clinical Therapy for Tendon Injury. J Cytokine Biol 7: 406.

Copyright: © 2022 Berglund AK. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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