Good news! But this research seems rather confusing or confused!
"... Researchers studied the effects of scratching by applying allergens to mice ears to cause a type of skin inflammation called dermatitis.
Some mice wore a tiny “cone of shame” to prevent scratching, while others were able to scratch their ears as they pleased.
The rodents that scratched showed more inflamed ears, with a higher immune response, but they also had less Staphylococcus aureus, a harmful bacteria known for causing skin infections. The study shows “that the act of scratching is really important” in producing more immune cells, wound healing ... With conditions that involve chronic itching, like psoriasis, scratching might only lead to further skin damage, the researchers say.
The study also dug into what goes on at the molecular level, finding previously unknown players in the itch-scratch cycle. As Aaron Ver Heul writes in a related Science Perspective, “beyond defining a previously unidentified neuroimmune itch-scratch circuit, the findings … may lay a foundation for discoveries to help people suffering from chronic itch.”"
From the editor's summary and structured abstract (unfortunately, the abstract is written for experts only and it seems vague, there is a heavy mix of skin disorders combined with temporary itches confusing the issue, clear separation seems missing):
"Editor’s summary
Itch, the sensation that stimulates scratching behavior, is often triggered by skin irritants and inflammation. Liu et al. found that ablating itch-sensing neurons or physically preventing scratching decreased the inflammation associated with antigen-dependent mast cell responses in response to chemicals that induce allergic immune responses ... Scratching promoted pain-sensing neurons to release a neuropeptide that stimulated mast cells, and this peptide hormone synergized with antigen-dependent activation to increase the mast cell’s degranulation and ability to produce inflammatory mediators. In a model of skin infection associated with antigen-specific mast cell responses, scratching contributed to decreasing the bacterial load. ...
Structured Abstract
INTRODUCTION
Scratching is an often irresistible, stereotypical, and evolutionarily conserved behavioral response to the sensation of cutaneous itch. In many common skin diseases, such as dermatitis (eczema), protracted itching—or pruritus—is the dominant symptom and represents a substantial source of morbidity. Scratching in response to itch is clinically well recognized to exacerbate dermatitis and is pathogenic in some diseases. However, scratching an itch is often a pleasurable sensation and does not trigger avoidance behavior, which suggests that it may provide some benefit to the host.
RATIONALE
In the skin, activated dermal mast cells mediate hallmarks of the cutaneous allergic response, including hives and itch, which results in scratching behavior. They also recruit inflammatory cells and promote host defense against Staphylococcus aureus. Mast cells can be activated through a variety of mechanisms, including allergens, that cross-link preformed complexes of immunoglobulin E (IgE) antibodies bound to the FcεRI receptor or via ligands for the MrgprB2 receptor, including substance P (SP)—a neuropeptide released by pain-sensing neurons. The functional consequence of mast cell activation through different receptors, how scratching promotes cutaneous inflammation, and whether scratching provides benefit to the host all remain poorly explored.
RESULTS
To explore the relationship between itch, scratching, and inflammation, we generated mice that allow for the selective and inducible ablation of the nonpeptidergic 2 (NP2) subset of itch-sensing neurons, characterized by the expression of MrgprA3 (called Mrgpra3DTR).
We found that MrgprA3-expressing neurons were required for scratching and inflammation in models of type 2 contact hypersensitivity and FcεRI-mediated mast cell activation. In both cases, scratching augmented mast cell degranulation, tumor necrosis factor (TNF) expression, and recruitment of neutrophils. Scratching was not required for increased expression of the alarmins thymic stromal lymphopoietin (TSLP) and interleukin-33 (IL-33), which are known to activate mast cells.
Rather, we found that scratching was sufficient to trigger release of SP from Trpv1-expressing neurons that synergized with FcεRI cross-linking, resulting in maximal TNF release from mast cells. This was confirmed using mice with a genetic ablation of MrgprB2 or the gene encoding SP (Tac1) and by chemogenetic inhibition of Trpv1-expressing neurons. Inflammation in mice prevented from scratching could be rescued by exogenous activation of Trpv1-expressing neurons. Finally, we found that scratching reduced cutaneous microbial diversity and, in an epicutaneous S. aureus infection model, both inflammation and host defense required scratching.
CONCLUSION
The itch-scratch cycle is a pathogenic process in allergic skin rashes, such as dermatitis, or arthropod reactions. In this cycle, itch and scratching increase inflammation and disease exacerbation.
Our data suggest that scratching activates cutaneous Trpv1-expressing neurons, which are a major source of SP in the skin. Coordinated activation of mast cells by both MrgprB2 and FcεRI agonism synergistically augments inflammation, in part through increased recruitment of neutrophils. Thus, dermal mast cells occupy a central node in cutaneous inflammation and are capable of integrating both adaptive and innate neuroimmune triggers.
Moreover, inflammation-induced scratching can reduce the abundance of certain members of the cutaneous commensal community and, in the context of superficial S. aureus infection, inflammation triggered by scratching provides enhanced host defense. These data exemplify how scratching can both exacerbate disease and benefit the host through a neuroimmune axis and reconciles the seemingly paradoxical role of scratching as a pathological process and evolutionary adaptation."
