12/10/2023
ABOUT HOW DIFFERENT SILKIES ARE COMPARED TO NORMAL CHICKENS (long read) IMMUNE SYSTEM AND FIBROMELANOTIC
Silkies are weird, their immune systems are different to that of normal chickens due to the crazy lots of black pigment (indeed eumelanin). Before the age of 10 weeks, Silkies are more prone to become ill due to immune deficiencies because of a less active immune system caused by the hyperpigmentation which spreads throughout tissues including immune organs like the bursa of fabricius and the spleen. This gives less immune response by B-lymphocytes (therefore lower titer after immunisation) later but another mechanism boosts the adaptive immune system only with time delay, i.e. after 10 weeks.
Therefore Silkies are not weaker in general just in another time frame compared to normal chickens, but this lack of B-lymphocytes is compensated by a higher amount of other innate defensines including mast cells and monocytes, near all blood vessels to act when necessary. When there is damage, pigmentation cumulates near the spot. The load of pigment in Silkies is considered part of the immune system of the Silkie.
Later, after the crucial first 10 weeks of the Silkie, due to the same hyperpigmentation the bursa of fabricius (known for innate chick immunity) and thymus degenerate much slower compared to normal chickens, and the Silkie benefits therefore from a longer from it. Due to the hyperpigmentation apoptosis (programmed cell death) of these organs goes much slower.
Next to this, at 24 weeks of age of the Silkie, there was more expression in the spleen of another group of immune cells giving more adapted immunity, these immune cells are in much lower quantities present in normal chickens. When the bursa of fabricius was finaly degenerated at the age of 23 weeks, special lymph nodes were detected in the intestines and spleen, adding to adaptive immunity.
Next question was how is all the black pigment distributed throughout the chicken, next to skin also along the blood vessels and even in the brain, lungs, te**is and ovaries.
First you might think, that in such a drenched-in-black bird the keratinocytes (featherpulpproductionfacilities in the skin) might also be black, hence the pulp too but as we know, white feathered Silkies exist, so the keratin producing cells themselves are not excluded from the hyperpigmentation but the feather pulp itself is.
How does all black pigment travel through the bird? The Silkie has a special motorway to distribute all pigment from the pigment cells (melanocytes) throughout and this motorway is a network of cells that spread their tentacles (imagine nerve cells' dendrites) to everywhere in the bird (motorway = filopodia). The filopodia are also used for communication between the pigment cells (melanocytes) and other cells in the body, for pigment delivery when considered necessary and to 'fill' the internal organs with pigment.
Pigment production continues to accelerate during maturation of the Silkie (as we can see that it takes often till 6 weeks before full melanisation of the toes is finished, but that is a layman's observation of course). It is proven that the melanisation in Silkies plays a large role in its immune system.
Furthermore a special thing about the Silkie is that the hyperpigmentation has influence on fertility. It is known that Silkies lay less, compared to Leghorn for instance. This is due to a cumulation of pigment in the egg follicles (secondary), more specific in the corpus luteum. Melanocytes in Silkie are also involved in the regulation of s*x hormone secretion and are therefore believed to delay the formation of ovarian follicles and therefore Silkies don't lay as many eggs as Leghorns in the peak of laying.
This is an old article, based on comments from breeders who know all about fibromelanosis and immune systems. I've written the above donald duck based on paper in link below for the ones who don't know everything (like me, lol, writing about it helps remembering).
[Ugly watermarks are against thieving digital creators]
All can be read in more detail in the 2015 paper:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0125686
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