Inflammatory process with CLL/SLL

[peacethruthestorm]

I was diagnosed with SLL/CLL 7/2021 and am on W&W. I generally feel well and stay very active walking 4-6 miles per day in addition to other activities. Four days ago the bottom portion of my right rib cage received a sudden jolt causing pain. The soreness has spread across my rib cage and I was having muscle spasms yesterday. There is no visible bruise, but I can feel that the area is inflamed and tenuous. The pain is with movement only, so I am pretty sure that the pain is musculoskeletal due to a bruised area as result of being at higher risk for bruising due to CLL following a traumatic event to the area.

I was reflecting on previous issues with back strains over the past few years (before my diagnosis) and how my inflammatory process always seemed to be more than it should be with those injuries. Prednisone was always the magic bullet to help calm the inflammation. It occurs to me now that this may be due to the high number of ineffective circulating B cells. Within a normal immune system response, the body is triggered by infection or injury to "send out the troops" to help repair damage from infection and/or injury. My theory is that when you have CLL, and the immune response is triggered fore either infection or injury the troops are sent to help, but many cells are ineffective in their efforts. A high number of B cells are sent to the area and with CLL you have too many to start with..... they try to rally (cause inflammation, etc.) to help, but they are unable to do their job. So, you are left with an exaggerated inflammatory response and it takes longer for the normal immune cells to take care of all the damage done by the initial injury and resulting inflammation.

Does anyone have an opinion or experience with this? I wondered about talking with my doctor about making prednisone available to me (to have on hand) to abort the inflammatory response for injuries such as this......if needed. I can tell pretty quickly when it would be necessary and am not one to overmedicate. Thoughts?

[Newdawn Administrator]

This is an immensely complex and interesting area but I do believe our dysfunctional immune systems and it’s individual components can create an abnormal response to inflammation. This is an excellent article on the subject entitled;

‘White blood cell conversations in chronic inflammation’ -

jonlieffmd.com/blog/white-b...

‘Chronic inflammation is different in multiple ways. Cancer has been called the “wound that doesn’t heal” because in the milieu of cancer, genetic pathways for repair of DNA activity is damaged and many more mutations can occur. These increased mutations help cancers and they interact with alterations in local cells where they switch allegiance and become supportive of the cancer rather than the normal tissue.

White blood cells are vital in all of these processes. But, only now has their role in chronic inflammation been found. This post will focus only on this new material and not the more widely known vital contribution of leukocytes in acute inflammation responses.’

Newdawn

[peacethruthestorm in reply to Newdawn]

Thank you for sharing. Interesting article.

[AussieNeil Administrator]

Per the reference Newdawn provided, it's the neutrophils that respond to injuries, not B cells. Neutrophils use our blood system for quick access to the injury site, then slip through capillary walls and follow a chemical trail (chemotaxis) released from damaged cells to find the location of the injury. It's the increase in neutrophils that causes the swelling and pinkness of the injured tissues.

B cells, including CLL cells, are active in the germinal centres in our ~500 lymph nodes. (CLL cells are dormant when in our blood. healthunlocked.com/cllsuppo... )

It's the macrophages (mature monocytes) that take invading bacteria, fungi, viruses, etc, from a wound to nearby nodes. There they present them to helper T cells which then help new B cells to mature into plasma cells that produce antibodies specific to any bugs that invaded through a cut or scratch. It's this adaptive immunity process of producing and selecting B cells with matching B Cell Receptors, then stimulating division of those B-cells, which causes our nodes to swell. One to two weeks later, these B-cells mature into plasma cells which continually release the matching part of the B Cell Receptor as free floating antibodies/immunoglobulins. These antibodies neutralise and mark for destruction any remaining invaders.

Active CLL cells in our nodes confuse our immune system by releasing messenger signals (cytokines) that drive our T cells to exhaustion, so they don't work well in that helper process by which our adaptive immune system responds. There are a number of other mechanisms by which our CLL cells confuse and reduce the effectiveness of our response to infections, so we can take longer to heal. CLL bone marrow infiltration can also reduce our neutrophil and monocyte production capacity.

CLL Society has a very good two part series on the use of steroids such as prednisone with CLL, commencing here:

cllsociety.org/2017/04/ster...

Neil

[Shrink in reply to AussieNeil]

Thank you Neil !!!